Nephrology — Acute Kidney Injury

101. Acute Kidney Injury (AKI)

pre-renal vs intrinsic (ATN/AIN) vs post-renal · KDIGO stage by Cr/UOP · find & reverse cause · stop nephrotoxins · dialyze for AEIOU · Super Compact

Sx: often asymptomatic (lab dx) · ↓urine output (oliguria <0.5 mL/kg/h), edema/volume overload, or signs of cause (hypotension/sepsis, obstruction) · advanced: uremic Sx (nausea, confusion, asterixis), volume overload/dyspnea (AKI is a Cr/UOP diagnosis — the syndrome is found, not felt)

Neg: denies chronic ↓GFR/small kidneys/anemia/renal osteodystrophy (CKD baseline — confirm baseline Cr) · denies anuria + flank pain/distended bladder (obstruction — bladder scan) · denies recent drug + rash/eosinophilia (AIN) · denies pigmenturia + ↑CK (rhabdo)

SHx: NSAID/herbal/contrast/nephrotoxic drug exposure · alcohol (volume/rhabdo) · IVDU · recent illness/diarrhea/poor intake (pre-renal)

Etiology: pre-renal (~most common — hypovolemia, sepsis, CHF/cirrhosis low EAV, NSAIDs/ACEi hemodynamic) · intrinsic: ATN (ischemic from prolonged pre-renal/sepsis, or nephrotoxic — aminoglycosides, contrast, pigment, myeloma), AIN (drugs), GN, vascular · post-renal (obstruction — BPH, stones, malignancy)

RF: CKD · age · diabetes/HTN · heart failure/cirrhosis · sepsis · nephrotoxin exposure · recent contrast/surgery

Data: BMP (↑Cr — KDIGO: ↑≥0.3 in 48h or ≥1.5× baseline in 7d; K — check first, treat hyperkalemia emergently; bicarbonate) · UOP (KDIGO: <0.5 mL/kg/h ×6–12h) · urinalysis + microscopy (bland=pre/post-renal; muddy brown granular casts=ATN; WBC/eos casts=AIN; RBC casts/dysmorphic RBC=GN; heme+ no RBC=myoglobin/hemoglobin) · urine lytes — FENa (<1% pre-renal, >2% ATN; FEUrea <35% if on diuretics) · urine protein/Cr · renal US (hydronephrosis=obstruction; small echogenic=CKD; size) · bladder scan/post-void residual (exclude retention) · CK (rhabdo) · consider CBC/smear, complement, ANA/ANCA, SPEP/light chains if intrinsic

DDx: CKD (vs acute) (baseline Cr, small kidneys, anemia/↑PTH) · pre-renal vs ATN (FENa, casts, response to fluids) · obstruction (hydronephrosis, bladder scan) · AIN/GN/vascular (urine sediment, serologies)

Home Meds: STOP nephrotoxins — NSAIDs, aminoglycosides, IV contrast (hold), vancomycin (level-adjust) · hold ACEi/ARB + diuretics if pre-renal/hypovolemic (resume when stable) · renally dose-adjust ALL meds to current GFR · hold metformin (lactic acidosis/contrast), SGLT2i

Plan

CONSULT: Nephrology (severe/unclear AKI, intrinsic disease, dialysis need) · Urology (obstruction needing decompression) · ICU (if dialysis/instability)

– First, exclude/treat life threats: check K immediately — hyperkalemia with ECG changes → calcium gluconate 1–2 g IV (membrane stabilization), insulin 10 units IV + D50 25 g, albuterol 10–20 mg neb, then K removal (furosemide if making urine, GI binder — patiromer/SZC, or dialysis); treat severe acidosis and volume overload
– Determine category (pre/intrinsic/post): volume exam + urinalysis/microscopy + FENa/FEUrea + renal US + bladder scan
– Pre-renal: restore perfusion — IV isotonic crystalloid (balanced/LR or NS) bolus if hypovolemic, reassess; treat sepsis (fluids + source control + antibiotics), optimize cardiac output in CHF, hold offending hemodynamic agents (NSAIDs/ACEi)
– ATN: supportive — remove nephrotoxin/treat ischemia, maintain euvolemia and perfusion, avoid further insults; no proven pharmacologic cure — most recover over days–weeks if supported
– Post-renal: relieve obstruction — bladder catheter for retention; nephrostomy/ureteral stent (urology/IR) for upper-tract; watch post-obstructive diuresis (replace ~half urine output, monitor electrolytes)
– Intrinsic (AIN/GN/vascular): stop culprit drug (AIN), nephrology workup + serologies, treat underlying disease
– Supportive throughout: stop all nephrotoxins, renally dose every drug, avoid contrast, manage volume/electrolytes/acid-base, nutrition; strict I&Os + daily weights
– Dialysis indications — "AEIOU": Acidosis refractory · Electrolytes (refractory hyperkalemia) · Ingestions (dialyzable toxin) · Overload (refractory volume) · Uremia (encephalopathy, pericarditis, bleeding)
– Always exclude obstruction (bladder scan + renal US) early — it's the most reversible cause and a missed Foley-treatable retention is a classic miss.
– PT/OT: mobilize; fall precautions if uremic/encephalopathic
– Trend daily: Cr/BUN/eGFR, K + other electrolytes, bicarbonate, UOP, daily weight, fluid balance, drug levels (vanc, etc.)
– Escalation triggers: hyperkalemia/ECG changes, refractory acidosis or overload, or uremic complications (pericarditis, encephalopathy) → urgent dialysis + nephrology; rising Cr despite measures → reassess category, consider biopsy
– Discharge checklist: cause documented + reversible factors corrected; nephrotoxins discontinued; meds re-dosed to recovering GFR (resume ACEi/ARB when stable); follow-up Cr in days; nephrology follow-up if not recovered; contrast-avoidance note; return precautions (decreased urine, swelling, confusion, dyspnea)

101. Acute Kidney Injury (AKI)

complete reference · pre-renal + ATN + medication-induced + obstructive · KDIGO staging · category-directed therapy · Full Card

Symptoms / Associated Sx

• Frequently asymptomatic and detected on laboratory testing; decreased urine output (oliguria <0.5 mL/kg/h) or anuria may be present

• Signs of the underlying cause: hypotension/sepsis, volume depletion, or features of obstruction (suprapubic fullness, flank pain)

• Volume overload (edema, dyspnea) and, when advanced, uremic symptoms — nausea, anorexia, confusion, asterixis, pericardial rub

Neg

• Pt denies a chronically reduced GFR, small echogenic kidneys, longstanding anemia, or renal osteodystrophy — argues against chronic kidney disease as the baseline (always establish the baseline creatinine to separate acute from chronic)

• Pt denies anuria with flank pain or a distended bladder — argues against obstructive uropathy (confirm with a bladder scan and renal ultrasound)

• Pt denies a recent culprit drug with rash/eosinophilia (AIN) and denies pigmenturia with elevated CK (rhabdomyolysis) — narrows the intrinsic causes

Social History (SHx)

• NSAID, herbal/supplement, iodinated contrast, or other nephrotoxic drug exposure

• Alcohol use (volume depletion, rhabdomyolysis)

• Recent illness with diarrhea/vomiting or poor oral intake (pre-renal)

• Injection drug use (endocarditis-related GN, infection)

Main Etiology

• Pre-renal (the most common category): true hypovolemia (hemorrhage, GI losses, poor intake), sepsis/distributive shock, reduced effective arterial volume in heart failure and cirrhosis, and hemodynamic agents (NSAIDs constrict the afferent arteriole; ACEi/ARB dilate the efferent arteriole)

• Intrinsic — acute tubular necrosis (ATN): ischemic (prolonged pre-renal or sepsis) or nephrotoxic (aminoglycosides, iodinated contrast, pigment from myoglobin/hemoglobin, myeloma light chains)

• Intrinsic — other: acute interstitial nephritis (drugs), glomerulonephritis, and vascular causes (atheroemboli, thrombotic microangiopathy)

• Post-renal (obstruction): bladder outlet obstruction from BPH, bilateral ureteral stones, or pelvic/retroperitoneal malignancy

RF

• Modifiable: nephrotoxin and contrast exposure, volume status, blood pressure/perfusion optimization, timely relief of obstruction

• Non-modifiable: chronic kidney disease, advanced age, diabetes, hypertension, heart failure, cirrhosis, recent major surgery

Data

• BMP (rising creatinine — KDIGO criteria: increase ≥0.3 mg/dL within 48h or ≥1.5× baseline within 7 days; check potassium first and treat hyperkalemia emergently; bicarbonate for metabolic acidosis; BUN:Cr ratio >20 suggests pre-renal)

• Urine output (KDIGO: <0.5 mL/kg/h for 6–12h is stage 1; lower thresholds/longer duration define higher stages)

• Urinalysis with microscopy (bland sediment in pre-renal and post-renal; muddy brown granular casts in ATN; white cells and white-cell/eosinophil casts in AIN; dysmorphic RBCs and RBC casts in glomerulonephritis; heme-positive dipstick without RBCs suggests myoglobin or hemoglobin)

• Urine electrolytes — FENa (<1% suggests pre-renal, >2% suggests ATN; use FEUrea <35% when the patient is on diuretics, which invalidate FENa)

• Urine protein-to-creatinine ratio (quantify proteinuria; heavy proteinuria points to glomerular disease)

• Renal ultrasound (hydronephrosis indicates obstruction; small echogenic kidneys indicate chronicity; assesses size and symmetry)

• Bladder scan / post-void residual (exclude urinary retention — a rapidly reversible cause)

• CK (rhabdomyolysis as a cause of pigment ATN)

• Targeted intrinsic workup when indicated (CBC and smear, C3/C4, ANA, ANCA, anti-GBM, SPEP/serum free light chains, hepatitis serologies)

DDx

Chronic kidney disease vs acute injury (baseline creatinine, small kidneys, anemia, elevated PTH favor chronicity) · pre-renal vs ATN (FENa, urinary casts, response to a fluid challenge) · obstruction (hydronephrosis, elevated post-void residual) · AIN / glomerulonephritis / vascular (urine sediment and serologies)

Home Meds

• Stop nephrotoxins: NSAIDs, aminoglycosides; hold iodinated contrast; adjust vancomycin by levels

• Hold: ACE inhibitors/ARBs and diuretics if pre-renal or hypovolemic, resuming once stable

• Renally dose-adjust all medications to the current (not baseline) GFR

• Hold: metformin (lactic acidosis risk, and around contrast) and SGLT2 inhibitors during acute illness

Plan

CONSULT: Nephrology (severe or unexplained AKI, intrinsic disease, dialysis need) · Urology/IR (obstruction requiring decompression) · ICU (dialysis or hemodynamic instability)

• Address immediate life threats first: check potassium urgently — for hyperkalemia with ECG changes, give calcium gluconate 1–2 g IV (cardiac membrane stabilization), insulin 10 units IV with dextrose 25 g (D50), and albuterol 10–20 mg nebulized to shift potassium, then remove potassium (loop diuretic if urine output is preserved, a GI cation binder such as patiromer or sodium zirconium cyclosilicate, or dialysis); also treat severe metabolic acidosis and symptomatic volume overload

• Determine the category (pre-renal, intrinsic, post-renal) with a volume exam, urinalysis and microscopy, FENa/FEUrea, renal ultrasound, and bladder scan

• Pre-renal: restore perfusion — isotonic crystalloid (balanced solution/lactated Ringer's or normal saline) boluses when hypovolemic with reassessment; treat sepsis with fluids, source control, and antibiotics; optimize cardiac output in heart failure; and hold hemodynamic offenders (NSAIDs, ACEi/ARB)

• ATN: supportive care — remove the nephrotoxin or treat the ischemic insult, maintain euvolemia and renal perfusion, and avoid additional insults; there is no proven pharmacologic cure, and most cases recover over days to weeks with good support

• Post-renal: relieve the obstruction — a bladder catheter for retention, or percutaneous nephrostomy/ureteral stenting (urology or IR) for upper-tract obstruction; anticipate post-obstructive diuresis and replace roughly half of the urine output while monitoring electrolytes

• Intrinsic (AIN, glomerulonephritis, vascular): stop the culprit drug for AIN, pursue a nephrology workup with serologies, and treat the underlying disease (often with immunosuppression)

• Supportive throughout: discontinue all nephrotoxins, renally dose every medication, avoid iodinated contrast, manage volume/electrolytes/acid-base, attend to nutrition, and follow strict intake/output with daily weights

• Dialysis indications (mnemonic AEIOU): refractory Acidosis; Electrolyte derangement (refractory hyperkalemia); Ingestions (dialyzable toxins/drugs); fluid Overload refractory to diuretics; and Uremic complications (encephalopathy, pericarditis, bleeding)

• PT/OT: early mobilization with fall precautions if uremic or encephalopathic

• Trend daily: creatinine/BUN/eGFR, potassium and other electrolytes, bicarbonate, urine output, daily weight, fluid balance, and relevant drug levels

• Escalation triggers: hyperkalemia with ECG changes, refractory acidosis or volume overload, or uremic pericarditis/encephalopathy → urgent dialysis and nephrology; a continued rise in creatinine despite appropriate measures → reassess the category and consider renal biopsy

• Discharge checklist: documented cause with reversible factors corrected; nephrotoxins discontinued; medications re-dosed to the recovering GFR (resume ACEi/ARB once stable); a follow-up creatinine within days; nephrology follow-up if not fully recovered; a contrast-avoidance note; return precautions for decreased urine output, swelling, confusion, or dyspnea

Red Flags

• Hyperkalemia with ECG changes (peaked T waves, widened QRS) → calcium, insulin/dextrose, and potassium removal; can be rapidly fatal

• Refractory acidosis, volume overload, or uremic pericarditis/encephalopathy → urgent dialysis

• Anuria → think obstruction (bilateral or of a single functioning kidney) or a major vascular/cortical event

• RBC casts/dysmorphic RBCs with AKI → rapidly progressive glomerulonephritis — a nephrologic emergency requiring prompt workup and often biopsy

• AKI with hypercalcemia, anemia, and bone pain → consider myeloma (cast nephropathy)

Senior IM Resident Pearls

• Potassium and obstruction first. Before the elegant workup, check the potassium (treat it) and exclude obstruction with a bladder scan and ultrasound — the two things that kill or are instantly reversible.

• The urine microscopy is the cheapest renal biopsy. Muddy brown granular casts = ATN; RBC casts = GN; WBC casts/eosinophils = AIN; bland sediment = pre-renal or post-renal. Look at it yourself.

• FENa lies on diuretics. A loop diuretic forces sodium out and falsely raises FENa — switch to FEUrea (<35% suggests pre-renal) in diuretic-treated patients.

• BUN:Cr >20 with bland urine points pre-renal; pair it with the volume exam and the fluid-challenge response rather than trusting one number.

• Re-dose to the current GFR, not the chart. Using a stale baseline creatinine to dose vancomycin or DOACs in evolving AKI causes toxicity — and stop metformin.

• Watch for post-obstructive diuresis after relieving obstruction — patients can lose liters and become hypovolemic and hypokalemic; replace about half the output and monitor electrolytes.

• Common mistake: reflexively bolusing fluid into every AKI — in cardiorenal or already-overloaded patients, more fluid worsens things; match the therapy to the category.

Nephrology — End-Stage Renal Disease

102. End-Stage Renal Disease (ESRD) Requiring Dialysis

missed dialysis / uremia / hyperkalemia / volume overload · the emergency is usually K or fluid · urgent HD per indication · protect access · Super Compact

Sx: after missed dialysis — dyspnea/orthopnea (volume overload, pulmonary edema), peripheral edema · hyperkalemia (weakness, palpitations, arrhythmia) · uremic Sx (nausea, fatigue, confusion, pruritus, asterixis) · pericardial rub (uremic pericarditis) (the lethal trio after a missed session: hyperkalemia, volume overload, severe uremia)

Neg: denies new focal infection/access erythema (access infection — examine) · denies chest pain + ECG ischemia (ACS — common in ESRD) · denies fever + pericardial rub/effusion w/ tamponade (uremic vs purulent pericarditis) · denies anuria-new + obstruction (residual function loss)

SHx: dialysis modality + schedule + last session + missed sessions · dry weight + access type (AVF/AVG/catheter) · tobacco · adherence/dietary K/fluid · transplant status

Etiology: irreversible loss of renal function (CKD G5, eGFR <15) on renal replacement; common ESRD causes — diabetes (#1), hypertension, glomerulonephritis, PKD; acute decompensation usually from missed/inadequate dialysis → fluid + K + uremic toxin accumulation

RF: diabetes/HTN · nonadherence to dialysis/diet · high interdialytic weight gain · dietary K/fluid indiscretion · intercurrent illness

Data: BMP — K first (hyperkalemia is the immediate killer; bicarbonate — acidosis; Ca/PO4; BUN/Cr context only — they're chronically high) · ECG (peaked T, wide QRS, sine wave = hyperK emergency; ischemia) · CBC (anemia of CKD; leukocytosis=infection) · Mg/phosphate · CXR (pulmonary edema, effusions, cardiomegaly) · troponin (interpret vs chronic elevation/baseline) · blood cultures + access exam (if febrile — catheter bacteremia) · weight vs dry weight · consider POCUS (volume, effusion)

DDx: volume overload vs pneumonia/sepsis (CXR, exam, cultures) · hyperkalemic arrhythmia vs primary cardiac (ECG, K) · uremic vs purulent/viral pericarditis (fever, cultures, effusion) · access infection/bacteremia (cultures, access exam)

Home Meds: continue phosphate binders (sevelamer/calcium acetate w/ meals), active vit D, ESA (epoetin/darbepoetin), antihypertensives (hold if hypotensive pre-HD) · renally dose/avoid renally-cleared drugs · protect the access arm (no BP/IV/venipuncture in fistula arm)

Plan

CONSULT: Nephrology (urgent — arrange dialysis, manage ESRD) · Cardiology (if ACS/pericardial tamponade) · Vascular/IR (access issues) · ICU (unstable/tamponade)

– Treat hyperkalemia emergently (most common immediate threat): ECG; if K high or ECG changes → calcium gluconate 1–2 g IV (stabilize membrane, repeat as needed), insulin 10 units IV + D50 25 g (recheck glucose — hypoglycemia risk in ESRD), albuterol 10–20 mg neb; definitive removal in anuric ESRD = dialysis (binders/diuretics have limited role; loop diuretics ineffective if anuric)
– Volume overload / pulmonary edema: sit up, O2, ± nitroglycerin/BiPAP for distress; urgent ultrafiltration via dialysis is the definitive therapy (loop diuretics often ineffective in ESRD); avoid large fluid administration
– Arrange urgent dialysis for the indication present (hyperkalemia, overload, severe acidosis, uremic pericarditis/encephalopathy, dialyzable ingestion)
– Severe acidosis: dialysis; bicarbonate only as a temporizing bridge if needed
– Uremic pericarditis: intensify dialysis (often daily, heparin-free given hemorrhagic risk); monitor for effusion/tamponade → echo, pericardiocentesis if tamponade
– Infection workup if febrile: blood cultures (peripheral + from catheter), examine access; empiric vancomycin (dosed for ESRD/HD) + gram-negative coverage (cefepime) pending cultures for suspected catheter bacteremia
– Manage chronic issues: continue phosphate binders, ESA, vitamin D; address anemia, mineral-bone disease; reconcile/renally dose meds
– The access arm is the patient's lifeline — document "no BP, no venipuncture, no IV in the fistula/graft arm" on admission; a thrombosed access from a stray BP cuff is a preventable disaster.
– PT/OT: mobilize as tolerated; fall precautions if uremic
– Trend: K + ECG, volume status/weight, bicarbonate, glucose (post-insulin), infection markers/cultures, response to dialysis
– Escalation triggers: hyperkalemic ECG changes, refractory pulmonary edema, tamponade physiology, or hemodynamic instability → emergent dialysis/ICU/pericardiocentesis
– Discharge checklist: dialysis resumed on schedule + adherence counseling (diet K/fluid, interdialytic weight goal); access functioning + protection documented; meds reconciled (binders, ESA, vit D, renally dosed); transplant referral status; nephrology + access follow-up; return precautions (dyspnea, weakness/palpitations, chest pain, fever, access redness/bleeding)

102. End-Stage Renal Disease (ESRD) Requiring Dialysis

complete reference · missed dialysis + uremia + electrolyte abnormalities · urgent dialysis + access protection · Full Card

Symptoms / Associated Sx

• After a missed or inadequate dialysis session: dyspnea, orthopnea, and peripheral edema from volume overload and pulmonary edema

• Hyperkalemia: muscle weakness, palpitations, and life-threatening arrhythmias (often with few symptoms until severe)

• Uremic symptoms: nausea, anorexia, fatigue, confusion, pruritus, asterixis; a pericardial friction rub suggests uremic pericarditis

Neg

• Pt denies a new focal infection or access-site erythema/tenderness — argues against access infection or catheter bacteremia (always examine the access)

• Pt denies chest pain with ischemic ECG changes — cardiovascular disease is the leading cause of death in ESRD, so exclude ACS

• Pt denies fever with a pericardial rub/effusion and tamponade physiology — distinguishes uremic pericarditis from purulent/viral causes and identifies tamponade

Social History (SHx)

• Dialysis details: modality (hemodialysis vs peritoneal), schedule, date of last session, and any missed sessions

• Dry weight and access type (arteriovenous fistula, graft, or tunneled catheter)

• Adherence to diet (potassium, fluid, phosphate) and the interdialytic weight gain pattern

• Tobacco use; transplant candidacy/waitlist status

Main Etiology

• Irreversible loss of kidney function (CKD stage G5, eGFR <15 mL/min/1.73m²) treated with renal replacement therapy

• Common causes of ESRD: diabetes mellitus (the leading cause), hypertension, glomerulonephritis, and polycystic kidney disease

• Acute decompensation is usually precipitated by missed or inadequate dialysis, leading to accumulation of fluid, potassium, and uremic toxins; dietary indiscretion and intercurrent illness contribute

RF

• Modifiable: dialysis and dietary adherence, interdialytic weight gain, fluid and potassium intake

• Non-modifiable: underlying diabetes/hypertension, loss of residual renal function, intercurrent illness

Data

• BMP — potassium first (hyperkalemia is the immediate life threat; bicarbonate for metabolic acidosis; calcium and phosphate; BUN/creatinine provide context only, as they are chronically elevated)

• ECG (peaked T waves, widened QRS, and a sine-wave pattern indicate a hyperkalemic emergency; also evaluate for ischemia)

• CBC (anemia of chronic kidney disease; leukocytosis suggests infection)

• Magnesium and phosphate (mineral and bone disease, repletion or restriction)

• Chest radiograph (pulmonary edema, pleural effusions, cardiomegaly/pericardial silhouette)

• Troponin (interpret against the patient's chronically elevated baseline)

• Blood cultures (peripheral and from the catheter) with a thorough access exam (febrile patients — catheter-related bacteremia)

• Current weight versus documented dry weight; point-of-care ultrasound (volume status, pericardial/pleural effusion)

DDx

Volume overload vs pneumonia/sepsis (chest radiograph, exam, cultures) · hyperkalemic arrhythmia vs primary cardiac event (ECG, potassium) · uremic vs purulent/viral pericarditis (fever, cultures, effusion) · access infection/bacteremia (cultures, access examination)

Home Meds

• Continue: phosphate binders (sevelamer or calcium acetate with meals), active vitamin D, erythropoiesis-stimulating agents (epoetin/darbepoetin), and antihypertensives (hold if hypotensive pre-dialysis)

• Renally dose or avoid: renally cleared medications; account for dialysis clearance

• Protect the access arm: no blood pressure measurement, IV placement, or venipuncture in the fistula/graft arm

Plan

CONSULT: Nephrology (urgent — arrange dialysis and manage ESRD) · Cardiology (ACS or pericardial tamponade) · Vascular surgery/IR (access complications) · ICU (instability or tamponade)

• Treat hyperkalemia emergently (the most common immediate threat): obtain an ECG; for an elevated potassium or any ECG changes, give calcium gluconate 1–2 g IV to stabilize the cardiac membrane (repeat as needed), insulin 10 units IV with dextrose 25 g (D50) to shift potassium (recheck glucose given the heightened hypoglycemia risk in ESRD), and albuterol 10–20 mg nebulized; definitive removal in an anuric patient is dialysis, since loop diuretics are ineffective without urine output and binders act slowly

• Volume overload/pulmonary edema: upright positioning, oxygen, and nitroglycerin/BiPAP for respiratory distress; urgent ultrafiltration via dialysis is the definitive therapy because loop diuretics are often ineffective in ESRD; avoid administering large fluid volumes

• Arrange urgent dialysis for the specific indication present — hyperkalemia, volume overload, severe acidosis, uremic pericarditis or encephalopathy, or a dialyzable ingestion

• Severe metabolic acidosis: treat with dialysis; use IV bicarbonate only as a temporizing bridge if needed

• Uremic pericarditis: intensify dialysis (often daily and heparin-free given the bleeding risk) and monitor for effusion and tamponade with echocardiography, proceeding to pericardiocentesis for tamponade

• If febrile: draw blood cultures from a peripheral site and the catheter, examine the access, and start empiric vancomycin (dosed for hemodialysis) plus gram-negative coverage (cefepime) pending cultures for suspected catheter-related bacteremia

• Manage chronic issues: continue phosphate binders, ESAs, and vitamin D; address anemia and mineral-bone disease; reconcile and renally dose all medications

• PT/OT: mobilize as tolerated with fall precautions if uremic

• Trend: potassium with serial ECGs, volume status and weight, bicarbonate, glucose after insulin, infection markers and cultures, and the response to dialysis

• Escalation triggers: hyperkalemic ECG changes, refractory pulmonary edema, tamponade physiology, or hemodynamic instability → emergent dialysis, ICU, or pericardiocentesis

• Discharge checklist: dialysis resumed on schedule with adherence counseling (potassium/fluid restriction, interdialytic weight goal); a functioning, protected access documented; medications reconciled (binders, ESA, vitamin D, renally dosed agents); transplant referral status addressed; nephrology and access follow-up; return precautions for dyspnea, weakness/palpitations, chest pain, fever, or access redness/bleeding

Red Flags

• Hyperkalemia with ECG changes → calcium, insulin/dextrose, albuterol, and urgent dialysis; can be rapidly fatal

• Flash pulmonary edema from volume overload → urgent ultrafiltration; diuretics usually ineffective

• Uremic pericarditis with a large effusion or tamponade → echocardiography and pericardiocentesis; dialyze heparin-free

• Fever with a tunneled catheter → catheter-related bloodstream infection until proven otherwise; cultures and empiric antibiotics

• Thrombosed or bleeding access → vascular/IR emergency; protect the access arm from any instrumentation

Senior IM Resident Pearls

• The emergency is almost always potassium or fluid. A missed-dialysis patient who looks sick needs an immediate ECG and potassium, and the definitive fix for both hyperkalemia and overload in anuric ESRD is dialysis, not diuretics.

• Diuretics don't work without urine. Reaching for furosemide in an anuric ESRD patient wastes time — ultrafiltration removes the fluid.

• Recheck the glucose after insulin. ESRD patients clear insulin slowly and are prone to delayed, prolonged hypoglycemia after the hyperkalemia cocktail.

• Protect the access arm from minute one. Put the order in writing — a BP cuff or IV in a fistula arm can thrombose the access and cost the patient their lifeline.

• Troponin and BUN/Cr are "chronically abnormal." Interpret them against the patient's baseline, not standard reference ranges, to avoid being misled.

• Uremic pericarditis means under-dialysis — intensify dialysis (heparin-free) and watch for tamponade rather than treating it as idiopathic.

• Common mistake: giving generous IV fluids to a hypotensive ESRD patient — they have no way to excrete it; treat the underlying cause and use dialysis for volume.

Nephrology — Uremic Syndrome

103. Uremia

clinical syndrome of retained solutes · encephalopathy / pericarditis / severe azotemia · uremia = a dialysis indication · the number doesn't diagnose it, the patient does · Super Compact

Sx: encephalopathy (confusion, lethargy, asterixis, myoclonus, seizures), pericarditis (pleuritic chest pain, friction rub), platelet dysfunction/bleeding (ecchymoses, GI bleed) · nausea/anorexia/vomiting, pruritus, uremic fetor, restless legs, peripheral neuropathy (uremia is a clinical diagnosis — symptoms + signs in advanced kidney failure, not a BUN threshold)

Neg: denies other causes of AMS — infection/drugs/structural (sepsis, intoxication, stroke — workup) · denies primary pericardial cause (viral/bacterial/post-MI — fever, cultures) · denies other bleeding etiology (coagulopathy, anticoagulant, structural) · denies hypoglycemia/hyponatremia/hypercalcemia (metabolic AMS mimics)

SHx: known CKD/ESRD + dialysis status/missed sessions · medication adherence · alcohol/drugs (AMS mimic) · timeline of azotemia (acute vs chronic)

Etiology: accumulation of nitrogenous + other uremic retention solutes as GFR falls (usually advanced CKD/ESRD or severe AKI) → multisystem toxicity; uremic pericarditis (fibrinous, can be hemorrhagic → tamponade), uremic encephalopathy, uremic platelet dysfunction (qualitative — impaired aggregation/vWF interaction)

RF: advanced CKD/ESRD · missed/inadequate dialysis · acute severe AKI · catabolic states (↑ urea generation)

Data: BMP (severe azotemia — markedly ↑BUN/Cr; the level supports but doesn't define uremia) · CBC (anemia of CKD; platelets usually normal in number — dysfunction is qualitative) · ECG (pericarditis — diffuse changes less typical than viral; watch for effusion/tamponade signs; concurrent hyperK) · echocardiogram (pericardial effusion/tamponade if pericarditis) · Ca/PO4/PTH · coags (usually normal PT/PTT — bleeding is platelet-functional, bleeding time/PFA not routinely used) · workup to exclude mimics of AMS (glucose, Na, Ca, infection, tox screen, neuro imaging as indicated)

DDx: other encephalopathy (infectious/toxic/metabolic/structural — exclude) · non-uremic pericarditis (viral/bacterial/post-MI/autoimmune) · other bleeding diatheses (anticoagulant, DIC, structural) · hepatic encephalopathy (liver disease, ammonia)

Home Meds: hold anticoagulants/antiplatelets if bleeding (uremia adds platelet dysfunction) · avoid sedatives (worsen/mask encephalopathy) · renally dose all meds · continue ESRD meds (binders, ESA, vit D)

Plan

CONSULT: Nephrology (urgent — dialysis is the definitive treatment) · Cardiology (pericarditis/tamponade) · ICU (encephalopathy with airway risk, tamponade)

– Dialysis is the definitive therapy — uremic encephalopathy, pericarditis, and bleeding are all firm indications for urgent/intensified dialysis; arrange promptly
– First exclude reversible mimics of the presenting syndrome (infection, drugs, metabolic — glucose/Na/Ca, neuro imaging if focal) so you don't attribute a treatable problem to uremia
– Uremic encephalopathy: dialysis; supportive care, avoid sedatives, seizure precautions; correct contributing metabolic derangements
– Uremic pericarditis: intensify dialysis (often daily, heparin-free to avoid hemorrhagic conversion); NSAIDs/colchicine have limited role and bleeding/renal concerns; monitor for tamponade (echo) → pericardiocentesis or pericardial window if tamponade/large effusion
– Uremic bleeding (platelet dysfunction): dialysis (improves platelet function); for active bleeding/procedures — DDAVP (desmopressin) 0.3 mcg/kg IV/SC (rapid, transient — releases vWF), conjugated estrogens 0.6 mg/kg IV daily ×5 (slower onset, longer duration), correct anemia (transfuse to Hgb ~10 improves platelet-vessel interaction), cryoprecipitate if refractory; hold antiplatelets/anticoagulants
– Supportive: manage volume/electrolytes/acid-base, nutrition, treat anemia/mineral-bone disease
– Uremic platelet dysfunction is qualitative — the platelet count and PT/PTT are typically normal; don't transfuse platelets expecting benefit. DDAVP, dialysis, and correcting anemia are what work.
– PT/OT: mobilize when safe; fall/aspiration precautions if encephalopathic
– Trend: mental status, BUN/Cr response to dialysis, pericardial status (rub, echo, tamponade signs), bleeding/Hgb, electrolytes
– Escalation triggers: declining mental status/airway → ICU; tamponade physiology → emergent pericardiocentesis; uncontrolled bleeding → DDAVP + dialysis + transfusion; seizures → treat + dialyze
– Discharge checklist: dialysis plan established/intensified + adherence counseling; pericarditis/effusion resolution documented; bleeding controlled with reversible factors addressed; meds reconciled + renally dosed; nephrology follow-up; return precautions (confusion, chest pain, bleeding, dyspnea)

103. Uremia

complete reference · encephalopathy + pericarditis + bleeding + severe azotemia · dialysis-defining syndrome · Full Card

Symptoms / Associated Sx

• Uremic encephalopathy: confusion, lethargy, asterixis, myoclonus, and in severe cases seizures

• Uremic pericarditis: pleuritic chest pain with a pericardial friction rub; risk of hemorrhagic effusion and tamponade

• Uremic platelet dysfunction: easy bruising, mucosal and GI bleeding

• General: nausea, anorexia, vomiting, pruritus, uremic fetor, restless legs, and peripheral neuropathy

Neg

• Pt denies an alternative cause of altered mental status — infection, intoxication, or a structural/vascular event — which must be excluded before attributing encephalopathy to uremia

• Pt denies features of a non-uremic pericarditis (fever, viral prodrome, recent MI, autoimmune disease) — these have different management

• Pt denies another bleeding etiology (anticoagulant effect, DIC, structural lesion) and denies metabolic mimics of AMS (hypoglycemia, hyponatremia, hypercalcemia)

Social History (SHx)

• Known CKD/ESRD with dialysis modality and any missed sessions

• Medication adherence

• Alcohol or drug use (mimics of encephalopathy)

• Timeline of the azotemia (acute kidney injury vs chronic progression)

Main Etiology

• Accumulation of urea and numerous other uremic retention solutes as GFR declines, typically in advanced CKD/ESRD or severe AKI, producing multisystem toxicity

• Uremic pericarditis is a fibrinous (sometimes hemorrhagic) pericardial inflammation that can progress to tamponade

• Uremic bleeding reflects a qualitative platelet defect — impaired platelet aggregation and platelet–von Willebrand factor interaction — rather than thrombocytopenia

RF

• Modifiable: dialysis adequacy and adherence, control of catabolic stressors

• Non-modifiable: advanced CKD/ESRD, severe AKI

Data

• BMP (severe azotemia with markedly elevated BUN and creatinine; the absolute level supports but does not by itself define uremia, which is clinical)

• CBC (anemia of chronic kidney disease; the platelet count is typically normal because the defect is functional)

• ECG (uremic pericarditis often lacks the diffuse ST changes of viral pericarditis; watch for effusion/low voltage/electrical alternans and concurrent hyperkalemia)

• Echocardiogram (pericardial effusion and tamponade physiology when pericarditis is suspected)

• Calcium, phosphate, PTH (mineral and bone disease)

• Coagulation studies (PT/PTT are usually normal; the bleeding tendency is platelet-functional and bleeding time/PFA testing is not routinely used)

• Workup to exclude mimics of altered mental status (glucose, sodium, calcium, infectious workup, toxicology, and neuroimaging when focal signs are present)

DDx

Other encephalopathy (infectious, toxic, metabolic, or structural — must be excluded) · non-uremic pericarditis (viral, bacterial, post-MI, autoimmune) · other bleeding diatheses (anticoagulant effect, DIC, structural lesion) · hepatic encephalopathy (liver disease, elevated ammonia)

Home Meds

• Hold: anticoagulants and antiplatelets in the setting of bleeding (uremia compounds the platelet defect)

• Avoid: sedatives that worsen or mask encephalopathy

• Renally dose: all medications

• Continue: ESRD medications (phosphate binders, ESAs, vitamin D)

Plan

CONSULT: Nephrology (urgent — dialysis is the definitive treatment) · Cardiology (pericarditis or tamponade) · ICU (encephalopathy with airway risk, tamponade)

• Dialysis is the definitive therapy: uremic encephalopathy, pericarditis, and bleeding are all firm indications for urgent or intensified dialysis — arrange it promptly

• Exclude reversible mimics first (infection, drugs, and metabolic derangements such as hypoglycemia, hyponatremia, or hypercalcemia; neuroimaging for focal deficits) so a treatable problem is not misattributed to uremia

• Uremic encephalopathy: dialysis, supportive care, avoidance of sedatives, seizure precautions, and correction of contributing metabolic derangements

• Uremic pericarditis: intensify dialysis, typically daily and heparin-free to avoid hemorrhagic conversion of the effusion; NSAIDs and colchicine have a limited role given bleeding and renal concerns; monitor closely for tamponade with echocardiography and proceed to pericardiocentesis or a pericardial window for tamponade or a large effusion

• Uremic bleeding (platelet dysfunction): dialysis improves platelet function; for active bleeding or before procedures, give desmopressin (DDAVP) 0.3 mcg/kg IV/SC for a rapid but transient effect (releases von Willebrand factor), and conjugated estrogens 0.6 mg/kg IV daily for 5 days for a slower-onset, longer-lasting effect; correct anemia by transfusing toward a hemoglobin of ~10 g/dL (red cells improve platelet–vessel wall interaction); cryoprecipitate for refractory bleeding; hold antiplatelets and anticoagulants

• Supportive care: manage volume, electrolytes, and acid-base; attend to nutrition; and treat anemia and mineral-bone disease

• PT/OT: mobilize when safe, with fall and aspiration precautions if encephalopathic

• Trend: mental status, BUN/creatinine response to dialysis, pericardial status (rub, echocardiographic effusion, tamponade signs), bleeding and hemoglobin, and electrolytes

• Escalation triggers: declining mental status with airway compromise → ICU; tamponade physiology → emergent pericardiocentesis; uncontrolled bleeding → DDAVP, dialysis, and transfusion; seizures → treat and dialyze

• Discharge checklist: an established or intensified dialysis plan with adherence counseling; documented resolution of pericarditis/effusion; controlled bleeding with reversible factors addressed; reconciled and renally dosed medications; nephrology follow-up; return precautions for confusion, chest pain, bleeding, or dyspnea

Red Flags

• Uremic pericarditis with a large or hemorrhagic effusion → tamponade risk → echocardiography, heparin-free dialysis, pericardiocentesis

• Progressive encephalopathy, myoclonus, or seizures → urgent dialysis and airway protection

• Active uremic bleeding → DDAVP, dialysis, anemia correction; hold antithrombotics

• Concurrent hyperkalemia → treat emergently in parallel

• Focal neurologic signs → image the brain; do not assume uremia

Senior IM Resident Pearls

• Uremia is a clinical diagnosis, not a BUN number. Patients tolerate very different absolute values; treat the syndrome (encephalopathy, pericarditis, bleeding) rather than chasing a threshold.

• Dialyze uremic pericarditis heparin-free. Anticoagulation can convert a fibrinous effusion into a hemorrhagic one and precipitate tamponade.

• The platelet count is normal — don't transfuse platelets. Uremic bleeding is a functional defect; DDAVP, dialysis, correcting anemia, and conjugated estrogens are the effective tools.

• DDAVP works fast but fades fast (and tachyphylaxis develops); pair it with conjugated estrogens for durable effect around bleeding or procedures.

• Always exclude the mimics. Infection, drugs, and metabolic derangements cause the same picture — uremia is partly a diagnosis of exclusion in the encephalopathic dialysis patient.

• Common mistake: attributing new altered mental status to uremia and dialyzing without checking a glucose, sodium, calcium, or imaging — missing a treatable, non-renal cause.

Nephrology / Vascular — Dialysis Access

104. Dialysis Access Complications

clotted fistula/graft · infected catheter (bacteremia) · access malfunction · protect the access · catheter infection = blood cultures + abx ± line removal · Super Compact

Sx: clotted AVF/AVG: loss of thrill/bruit, no flow on dialysis, cool/pulseless access · infected catheter: fever/rigors (esp with dialysis), exit-site erythema/purulence, sepsis · malfunction: poor flows, recirculation, prolonged bleeding post-needling, arm swelling (central stenosis) · steal (hand pain/ischemia), aneurysm/pseudoaneurysm, high-output heart failure

Neg: denies alternate infection source (UTI/pneumonia/endocarditis — pan-culture, exam) · denies bleeding access w/ skin breakdown over aneurysm (impending rupture — emergency) · denies limb ischemia/steal (hand pallor/pain) · denies central stenosis missed (unilateral arm/face/breast swelling)

SHx: access type (AVF vs AVG vs tunneled catheter) + age/site + prior interventions · diabetes/PVD (steal, poor maturation) · prior catheter infections/bacteremia · anticoagulation

Etiology: thrombosis (stenosis at anastomosis/outflow, hypotension, hypercoagulable, extrinsic compression) · catheter-related bloodstream infection (tunneled catheters — biofilm; Staph aureus, coag-neg staph, gram-negatives) · stenosis/malfunction (neointimal hyperplasia, central venous stenosis from prior lines) · steal syndrome, aneurysm/pseudoaneurysm, high-output failure

RF: tunneled catheter (vs fistula) · diabetes/PVD · hypotension · prior central lines (central stenosis) · prior access failures

Data: exam (thrill/bruit, pulse, exit site, arm/face swelling, distal perfusion) · blood cultures ×2 (peripheral + through catheter) (catheter-related BSI dx) · CBC (leukocytosis) · lactate (sepsis) · access ultrasound / Doppler (thrombosis, stenosis, flow, aneurysm, maturation) · fistulogram (angiography) (define + treat stenosis/thrombosis — diagnostic + therapeutic) · echo (if S. aureus bacteremia — endocarditis; or high-output failure) · K/BMP (if access lost → can't dialyze → hyperkalemia risk)

DDx: catheter BSI vs other source (cultures, exam, imaging) · access thrombosis vs stenosis (Doppler/fistulogram) · steal syndrome (distal ischemia) · central venous stenosis (unilateral arm/face swelling)

Home Meds: continue anticoagulation if prescribed for access (weigh bleeding) · protect the access (no BP/IV/venipuncture in access arm) · renally/HD dose antibiotics · hold nephrotoxins

Plan

CONSULT: Interventional radiology / Vascular surgery (urgent — declot/angioplasty, access salvage) · Nephrology (dialysis plan, access strategy) · ID (complex/persistent bacteremia) · Cardiology (endocarditis/high-output failure)

– If access lost and dialysis is due: arrange dialysis via a temporary route (place a temporary HD catheter — e.g. internal jugular) while salvaging the permanent access; check K/volume — treat hyperkalemia/overload emergently if present (calcium gluconate 1–2 g IV + insulin 10 units IV + D50 25 g + albuterol neb for hyperkalemic ECG changes, then dialysis)
– Clotted AVF/AVG: urgent referral to IR/vascular for percutaneous (or surgical) thrombectomy/declot + angioplasty of underlying stenosis — best salvaged early (within 24–48h); identify and treat the culprit stenosis to prevent re-clot
– Catheter-related bloodstream infection: blood cultures (peripheral + catheter) before antibiotics → empiric vancomycin (dosed for HD, target trough/AUC) + gram-negative coverage (cefepime 2 g IV or gentamicin per protocol) → narrow to cultures; tunneled catheter removal if hemodynamic instability, persistent bacteremia >48–72h, metastatic infection, or virulent organism (S. aureus, Pseudomonas, Candida); catheter salvage with antibiotic lock only in selected stable cases; duration typically 2–3 wks (4–6 wks if complicated/endocarditis)
– S. aureus bacteremia: echocardiography (TEE) for endocarditis, ID consult, source control, prolonged therapy
– Stenosis/malfunction: fistulogram with angioplasty (± stent) of the stenotic segment; central venous stenosis (arm/face swelling) → venoplasty
– Steal syndrome (hand ischemia): vascular surgery — banding/DRIL/ligation depending on severity
– Aneurysm/pseudoaneurysm with skin breakdown or bleeding: vascular emergency — direct pressure, urgent surgery (rupture risk)
– Don't remove a tunneled catheter reflexively for every fever — culture first; but DO remove it promptly for instability, persistent bacteremia, or S. aureus/Pseudomonas/Candida, because biofilm won't clear with antibiotics alone.
– PT/OT: as tolerated; protect access arm
– Trend: access exam (thrill/bruit/flow), culture results + clearance, fever curve, K/volume if dialysis disrupted, distal perfusion
– Escalation triggers: sepsis/instability → ICU + line removal; access rupture/active bleeding → vascular emergency; failure to clear bacteremia → remove catheter + image for endocarditis/septic emboli; missed dialysis with hyperkalemia → emergent dialysis
– Discharge checklist: access salvaged or alternative plan + dialysis continuity confirmed; antibiotic course defined (duration, route, HD dosing); culture follow-up + clearance documented; access protection counseling; nephrology + vascular/IR follow-up; return precautions (fever, loss of thrill, access bleeding/swelling, hand pain)

104. Dialysis Access Complications

complete reference · clotted fistula/graft + infected catheter + malfunction · salvage + infection management · Full Card

Symptoms / Associated Sx

• Clotted AVF/AVG: loss of the palpable thrill and audible bruit, inability to achieve flow on dialysis, a cool or pulseless access

• Infected catheter: fever and rigors (often triggered during a dialysis run), exit-site erythema or purulence, and sepsis

• Malfunction: poor dialysis flows, increased recirculation, prolonged bleeding after needle removal, and ipsilateral arm/face swelling (central venous stenosis)

• Other: steal syndrome (hand pain, pallor, ischemia), aneurysm/pseudoaneurysm, and high-output heart failure from a high-flow access

Neg

• Pt denies an alternative infection source (UTI, pneumonia, endocarditis) — pan-culture and examine before attributing fever to the access

• Pt denies skin breakdown or bleeding over an access aneurysm — its presence signals impending rupture, a vascular emergency

• Pt denies distal limb ischemia/steal (hand pain, pallor) and denies unilateral arm/face/breast swelling (central venous stenosis)

Social History (SHx)

• Access type (arteriovenous fistula vs graft vs tunneled catheter), its age/site, and prior interventions

• Diabetes and peripheral vascular disease (steal syndrome, poor maturation)

• Prior catheter infections or bloodstream infections

• Anticoagulation status

Main Etiology

• Thrombosis: usually due to an underlying stenosis (at the anastomosis or venous outflow), hypotension, a hypercoagulable state, or extrinsic compression

• Catheter-related bloodstream infection: biofilm formation on tunneled catheters; common organisms are Staphylococcus aureus, coagulase-negative staphylococci, and gram-negative bacilli

• Stenosis/malfunction: neointimal hyperplasia at the venous anastomosis, and central venous stenosis from prior central catheters

• Other: steal syndrome (distal ischemia), aneurysm/pseudoaneurysm, and high-output cardiac failure

RF

• Modifiable: minimizing catheter use in favor of fistulas, avoiding hypotension, limiting central line placement

• Non-modifiable: diabetes/PVD, prior access failures, prior central venous catheterization

Data

• Focused exam (thrill and bruit, distal pulses and perfusion, exit-site appearance, and arm/face swelling)

• Blood cultures ×2 — peripheral and through the catheter (diagnosis of catheter-related bloodstream infection; differential time-to-positivity supports a catheter source)

• CBC and lactate (leukocytosis and sepsis severity)

• Access ultrasound/Doppler (thrombosis, stenosis, flow volume, aneurysm, and fistula maturation)

• Fistulogram (angiography) (defines and treats stenosis/thrombosis in the same setting — both diagnostic and therapeutic)

• Echocardiography (for S. aureus bacteremia to evaluate for endocarditis, or to assess high-output cardiac failure)

• BMP/potassium (if the access is lost and dialysis is interrupted, hyperkalemia and volume overload can develop)

DDx

Catheter bloodstream infection vs another source (cultures, exam, imaging) · access thrombosis vs stenosis (Doppler, fistulogram) · steal syndrome (distal ischemia) · central venous stenosis (unilateral arm/face swelling)

Home Meds

• Continue: anticoagulation if prescribed for the access, weighing bleeding risk

• Protect the access: no blood pressure, IV, or venipuncture in the access arm

• Dose antibiotics for hemodialysis; hold nephrotoxins

Plan

CONSULT: Interventional radiology/vascular surgery (urgent — declot, angioplasty, access salvage) · Nephrology (dialysis plan and access strategy) · Infectious Disease (complex or persistent bacteremia) · Cardiology (endocarditis or high-output failure)

• If the access is lost and dialysis is due: arrange dialysis through a temporary route (place a temporary hemodialysis catheter, typically internal jugular) while working to salvage the permanent access; check potassium and volume status and treat hyperkalemia or overload emergently — for hyperkalemic ECG changes give calcium gluconate 1–2 g IV, insulin 10 units IV with dextrose 25 g, and nebulized albuterol, then dialyze

• Clotted AVF/AVG: urgent referral to IR or vascular surgery for percutaneous or surgical thrombectomy/declot with angioplasty of the underlying stenosis; salvage rates are best when addressed early (within 24–48h), and the culprit stenosis must be treated to prevent re-thrombosis

• Catheter-related bloodstream infection: obtain peripheral and catheter blood cultures before antibiotics, then start empiric vancomycin (dosed for hemodialysis to an appropriate trough/AUC) plus gram-negative coverage (cefepime 2 g IV, or an aminoglycoside per protocol), narrowing to culture results; remove the tunneled catheter for hemodynamic instability, persistent bacteremia beyond 48–72h, metastatic infection, or a virulent organism (S. aureus, Pseudomonas, Candida); catheter salvage with an antibiotic lock is reserved for selected stable patients; treat for 2–3 weeks typically, or 4–6 weeks for complicated infection or endocarditis

• S. aureus bacteremia: echocardiography (transesophageal) to evaluate for endocarditis, ID consultation, source control, and prolonged therapy

• Stenosis/malfunction: fistulogram with angioplasty (with or without a stent) of the stenotic segment; for central venous stenosis with arm/face swelling, perform venoplasty

• Steal syndrome with hand ischemia: vascular surgery for banding, distal revascularization–interval ligation (DRIL), or ligation depending on severity

• Aneurysm/pseudoaneurysm with overlying skin breakdown or bleeding: a vascular emergency — apply direct pressure and obtain urgent surgical repair given the rupture risk

• PT/OT: as tolerated, protecting the access arm

• Trend: access exam (thrill, bruit, flows), culture results and clearance, fever curve, potassium and volume if dialysis is disrupted, and distal perfusion

• Escalation triggers: sepsis or instability → ICU and catheter removal; access rupture or active bleeding → vascular emergency; failure to clear bacteremia → remove the catheter and image for endocarditis/septic emboli; missed dialysis with hyperkalemia → emergent dialysis

• Discharge checklist: access salvaged or an alternative plan with dialysis continuity confirmed; a defined antibiotic course (duration, route, hemodialysis dosing); culture follow-up with documented clearance; access-protection counseling; nephrology and vascular/IR follow-up; return precautions for fever, loss of thrill, access bleeding or swelling, or hand pain

Red Flags

• Access aneurysm/pseudoaneurysm with skin breakdown or bleeding → impending rupture → vascular emergency

• S. aureus, Pseudomonas, or Candida catheter bacteremia, instability, or persistent positive cultures → remove the catheter and evaluate for endocarditis/metastatic infection

• Clotted access with missed dialysis and hyperkalemia → emergent dialysis via a temporary catheter

• Hand ischemia/steal → vascular surgery to prevent tissue loss

• High-output heart failure from a high-flow access → cardiology and access-flow reduction

Senior IM Resident Pearls

• Culture before you pull, but pull when you must. Don't yank every tunneled catheter for a single fever — culture first — but remove it promptly for instability, persistent bacteremia, or S. aureus/Pseudomonas/Candida, because biofilm defeats antibiotics alone.

• A clotted access is salvageable if you move fast. Early IR/vascular referral (within 24–48h) for declot plus angioplasty of the underlying stenosis saves the access — and always fix the stenosis, or it re-clots.

• Loss of thrill = thrombosis until proven otherwise. Auscultate and palpate every access; a missing thrill/bruit is an urgent finding.

• Unilateral arm or facial swelling is central venous stenosis from prior lines — it needs venoplasty, not diuretics.

• S. aureus in a dialysis patient earns an echo. The metastatic complication rate is high — get a TEE and ID on board.

• Protect the access arm relentlessly — the single most important nursing order in a dialysis admission.

• Common mistake: treating catheter bacteremia with antibiotics through the infected catheter and leaving it in a deteriorating patient — source control means removing the line.

Nephrology — Acute-on-Chronic Kidney Disease

105. Acute on Chronic Kidney Disease (AoCKD)

acute rise in Cr above a known CKD baseline · find the superimposed insult · CKD reduces reserve → smaller hits cause bigger swings · protect residual function · Super Compact

Sx: known CKD with a new acute deterioration — rising Cr, falling UOP, worsening volume overload/edema/dyspnea · may be asymptomatic (lab) · symptoms of the precipitant (sepsis, dehydration, obstruction) or of advancing uremia (the task: identify the acute insult on top of chronic disease)

Neg: denies that this is pure CKD progression (look for a reversible acute trigger) · denies obstruction (bladder scan/US) · denies new nephrotoxin/contrast (med review) · denies hypovolemia vs overload mislabel (volume exam — both occur in CKD)

SHx: CKD etiology + baseline Cr/eGFR (critical anchor) · diabetes/HTN · nephrotoxin exposure (NSAIDs, contrast, abx) · recent illness/volume loss · heart failure/cirrhosis

Etiology: a superimposed acute insult on CKD — pre-renal (volume loss, sepsis, NSAIDs/ACEi, cardiorenal), ATN (ischemic/nephrotoxic — contrast, drugs), obstruction (BPH, stones), AIN (drugs), or acute progression of the primary disease (GN flare); CKD lowers renal reserve so modest insults cause large Cr changes

RF: baseline CKD severity (lower eGFR = higher risk) · diabetes/HTN/proteinuria · nephrotoxins · heart failure/cirrhosis · recurrent AKI episodes

Data: BMP — compare to baseline Cr (quantify the acute rise vs documented baseline; K — treat hyperkalemia emergently; bicarbonate) · urinalysis + microscopy (casts — ATN/AIN/GN; bland — pre/post-renal) · FENa/FEUrea (less reliable in CKD but still informative; FEUrea if on diuretics) · urine protein/Cr (compare to baseline proteinuria; new rise → GN) · renal US (small echogenic = chronicity; hydronephrosis = obstruction; asymmetry) · bladder scan · Ca/PO4/PTH/Hgb (CKD-MBD/anemia — chronic markers) · drug levels · targeted serologies if intrinsic

DDx: pure CKD progression vs superimposed AKI (slope of Cr, reversible trigger) · pre-renal vs ATN vs obstruction vs AIN/GN (urine, US, FENa) · hyperkalemia/acidosis as presenting issue · cardiorenal (CHF + worsening renal fxn)

Home Meds: STOP nephrotoxins (NSAIDs, hold contrast); hold ACEi/ARB + diuretics during acute pre-renal insult (resume when stable — they're protective long-term) · renally re-dose ALL meds to current GFR (not baseline) · hold metformin/SGLT2i during acute illness

Plan

CONSULT: Nephrology (significant AoCKD, unclear cause, dialysis need, advanced CKD) · Urology (obstruction) · the relevant service for the precipitant (sepsis, CHF)

– First treat life threats: hyperkalemia (more dangerous and common in CKD) — calcium gluconate 1–2 g IV for ECG changes, insulin 10 units IV + D50 25 g, albuterol neb, then removal (loop diuretic if urine-making, GI binder — patiromer/SZC, or dialysis); manage severe acidosis/overload
– Anchor to the baseline: find the documented baseline Cr/eGFR and quantify the acute change — this defines the "acute-on-chronic" and frames urgency
– Identify and reverse the acute insult (don't write it off as "just progression"): volume status, urine microscopy, FENa/FEUrea, renal US, bladder scan, med review
– Pre-renal: careful isotonic fluid if hypovolemic (cautious — CKD patients overload easily), treat sepsis, optimize cardiac output, hold NSAIDs/ACEi temporarily
– ATN: remove nephrotoxin, maintain perfusion/euvolemia, supportive; avoid contrast and further insults
– Obstruction: relieve it — Foley for retention, stent/nephrostomy for upper tract; watch post-obstructive diuresis
– AIN/GN: stop culprit drug, nephrology + serologies, treat underlying disease
– Protect residual function: strict nephrotoxin avoidance, BP and glycemic control, renally dose everything, treat CKD complications (anemia, acidosis, mineral-bone disease)
– Dialysis if AEIOU: refractory Acidosis · Electrolytes (hyperK) · Ingestion · Overload · Uremia
– The whole game is separating the reversible acute insult from irreversible chronic decline — never accept "just CKD progression" without ruling out volume, obstruction, and nephrotoxins, the three you can actually fix today.
– PT/OT: mobilize; fall precautions if uremic
– Trend daily: Cr vs baseline, K + electrolytes, bicarbonate, UOP, weight/volume, drug levels
– Escalation triggers: hyperkalemic ECG changes, refractory overload/acidosis, uremic complications → dialysis + nephrology; failure to recover toward baseline → reassess, consider biopsy
– Discharge checklist: precipitant identified + corrected; recovery toward (or new) baseline documented; nephrotoxins stopped + meds re-dosed (resume ACEi/ARB when stable as they slow CKD); close outpatient Cr recheck; nephrology follow-up; CKD care (BP/glucose/diet, vaccines); return precautions (decreased urine, swelling, confusion, dyspnea)

105. Acute on Chronic Kidney Disease (AoCKD)

complete reference · superimposed acute insult on CKD · baseline anchoring · reversible-cause hunt + residual function protection · Full Card

Symptoms / Associated Sx

• Known chronic kidney disease with a new acute deterioration — a rising creatinine, falling urine output, and worsening volume overload (edema, dyspnea)

• Frequently asymptomatic and detected on labs

• Symptoms of the precipitating insult (sepsis, dehydration, obstruction) or of advancing uremia

Neg

• Pt denies that this is purely chronic progression — actively look for a reversible acute trigger rather than attributing the rise to CKD alone

• Pt denies obstruction (confirm with bladder scan and renal ultrasound) and denies a new nephrotoxin or contrast exposure (review the medication list)

• Pt denies a mislabeled volume state — both hypovolemia and overload occur in CKD, so the volume exam must be deliberate

Social History (SHx)

• CKD etiology and the documented baseline creatinine/eGFR (the critical anchor for interpreting the acute change)

• Diabetes and hypertension

• Nephrotoxin exposure (NSAIDs, iodinated contrast, antibiotics)

• Recent illness or volume loss; heart failure or cirrhosis

Main Etiology

• A superimposed acute insult on chronic kidney disease: pre-renal (volume loss, sepsis, NSAIDs/ACEi, cardiorenal), acute tubular necrosis (ischemic or nephrotoxic, including contrast and drugs), obstruction (BPH, stones), acute interstitial nephritis (drugs), or acute progression/flare of the primary kidney disease (e.g. glomerulonephritis)

• Reduced renal reserve in CKD means that comparatively modest insults produce disproportionately large changes in creatinine

RF

• Modifiable: nephrotoxin exposure, blood pressure and glycemic control, volume management

• Non-modifiable: baseline CKD severity (lower eGFR confers higher risk), diabetes/hypertension/proteinuria, heart failure/cirrhosis, and a history of recurrent AKI

Data

• BMP compared to the baseline creatinine (quantify the acute rise against the documented baseline; check potassium and treat hyperkalemia emergently; bicarbonate for acidosis)

• Urinalysis with microscopy (casts suggest ATN/AIN/glomerulonephritis; bland sediment suggests pre-renal or post-renal)

• FENa/FEUrea (less reliable in CKD but still informative; use FEUrea when the patient is on diuretics)

• Urine protein-to-creatinine ratio (compare to the baseline; a new rise suggests glomerular disease)

• Renal ultrasound (small echogenic kidneys confirm chronicity; hydronephrosis indicates obstruction; assess asymmetry)

• Bladder scan (exclude retention)

• Calcium, phosphate, PTH, hemoglobin (chronic markers of CKD–mineral bone disease and anemia)

• Drug levels and targeted serologies (when an intrinsic or drug-related cause is suspected)

DDx

Pure CKD progression vs a superimposed AKI (slope of creatinine, presence of a reversible trigger) · pre-renal vs ATN vs obstruction vs AIN/GN (urine microscopy, ultrasound, FENa) · hyperkalemia/acidosis as the presenting problem · cardiorenal syndrome (heart failure with worsening renal function)

Home Meds

• Stop nephrotoxins: NSAIDs; hold iodinated contrast

• Hold: ACE inhibitors/ARBs and diuretics during an acute pre-renal insult, resuming when stable (they are renoprotective long-term)

• Renally re-dose all medications to the current (not baseline) GFR

• Hold: metformin and SGLT2 inhibitors during acute illness

Plan

CONSULT: Nephrology (significant acute-on-chronic injury, unclear cause, dialysis need, advanced CKD) · Urology (obstruction) · the service relevant to the precipitant (sepsis, heart failure)

• Treat life threats first: hyperkalemia is more common and dangerous in CKD — give calcium gluconate 1–2 g IV for ECG changes, insulin 10 units IV with dextrose 25 g, and nebulized albuterol, then remove potassium (a loop diuretic if urine output is preserved, a GI cation binder such as patiromer or sodium zirconium cyclosilicate, or dialysis); manage severe acidosis and volume overload

• Anchor to the baseline: locate the documented baseline creatinine/eGFR and quantify the acute change, which defines the acute-on-chronic injury and frames urgency

• Identify and reverse the acute insult rather than dismissing it as progression — assess volume status, urine microscopy, FENa/FEUrea, renal ultrasound, bladder scan, and the medication list

• Pre-renal: careful isotonic fluid resuscitation if hypovolemic (cautiously, since CKD patients overload easily), treat sepsis, optimize cardiac output, and temporarily hold NSAIDs and ACEi/ARB

• ATN: remove the nephrotoxin, maintain perfusion and euvolemia, provide supportive care, and avoid contrast and additional insults

• Obstruction: relieve it with a bladder catheter for retention or a stent/nephrostomy for upper-tract obstruction, and anticipate post-obstructive diuresis

• AIN/glomerulonephritis: stop the culprit drug, involve nephrology with serologic testing, and treat the underlying disease

• Protect residual function: strict nephrotoxin avoidance, blood pressure and glycemic control, renal dosing of all medications, and treatment of CKD complications (anemia, acidosis, mineral-bone disease)

• Dialysis for AEIOU indications: refractory acidosis, electrolyte derangement (hyperkalemia), ingestions, fluid overload, or uremic complications

• PT/OT: mobilize with fall precautions if uremic

• Trend daily: creatinine against baseline, potassium and other electrolytes, bicarbonate, urine output, weight/volume status, and drug levels

• Escalation triggers: hyperkalemic ECG changes, refractory overload or acidosis, or uremic complications → dialysis and nephrology; failure to recover toward baseline → reassess and consider biopsy

• Discharge checklist: the precipitant identified and corrected; recovery toward (or a new) baseline documented; nephrotoxins stopped and medications re-dosed (resume ACEi/ARB once stable, as they slow CKD progression); a close outpatient creatinine recheck; nephrology follow-up; ongoing CKD care (blood pressure, glycemic, and dietary management, vaccinations); return precautions for decreased urine output, swelling, confusion, or dyspnea

Red Flags

• Hyperkalemia with ECG changes → emergent treatment; CKD patients reach dangerous levels quickly

• Refractory volume overload, acidosis, or uremic complications → dialysis

• RBC casts/new heavy proteinuria → a glomerular process superimposed on CKD → urgent nephrology and possible biopsy

• Anuria → obstruction or a major vascular event

• Rapid loss of residual function → aggressive reversible-cause workup before accepting it as progression

Senior IM Resident Pearls

• Find the baseline first. "Acute-on-chronic" is meaningless without the prior creatinine — the documented baseline turns a scary number into an interpretable change.

• Never accept "just CKD progression" until you've excluded the three reversible insults you can fix today — volume, obstruction, and nephrotoxins.

• CKD patients overload easily. They have reduced reserve in both directions — be deliberate with fluids, because the same patient can be dry one day and in flash pulmonary edema the next.

• Hyperkalemia is the early killer. A small acute insult on CKD can spike the potassium fast — check it and an ECG up front.

• Re-dose to the current GFR. Using the chronic baseline to dose drugs during an acute dip causes accumulation and toxicity.

• Hold the ACEi/ARB acutely, but resume it. It's protective long-term for proteinuric CKD — the temporary hold during a pre-renal insult shouldn't become permanent discontinuation.

• Common mistake: bolusing fluids reflexively — in cardiorenal or already-overloaded CKD patients, that worsens the kidney and the lungs; match therapy to the mechanism.

Nephrology / Acid-Base — Metabolic Acidosis

106. Metabolic Acidosis

low bicarb + low pH · anion gap splits the differential (HAGMA vs NAGMA) · check the gap, the delta-delta, and compensation · treat the cause · Super Compact

Sx: often the underlying illness dominates — Kussmaul (deep rapid) breathing (respiratory compensation), tachypnea · nausea/vomiting, abdominal pain, confusion/lethargy · signs of the cause (DKA — polyuria/dehydration; sepsis/shock — lactic; uremia — AKI/CKD) (severe acidemia → ↓cardiac contractility, arrhythmia, vasodilation/hypotension)

Neg: denies vomiting/NG loss/diuretics (would suggest metabolic alkalosis instead) · denies pure respiratory cause (check pCO2/compensation) · denies mixed disorder missed (use delta-delta + compensation formulas) · denies toxic alcohol exposure if unexplained HAGMA (osmolar gap)

SHx: diabetes (DKA) · alcohol (alcoholic ketoacidosis, toxic alcohols, lactic) · toxic ingestion (methanol/ethylene glycol, salicylate) · CKD/ESRD · diarrhea (NAGMA) · metformin (lactic)

Etiology / framework: HAGMA (↑ unmeasured anions) — "GOLD MARK": Glycols (ethylene glycol/propylene), Oxoproline, L-lactate, D-lactate, Methanol, Aspirin (salicylate), Renal failure (uremic acids), Ketoacidosis (DKA/AKA/starvation) · NAGMA (↑ Cl⁻) — "HARDASS": Hyperalimentation, Acetazolamide, RTA, Diarrhea (#1), Ammonium chloride, Spironolactone, Saline; common drivers per your list — AKI/CKD (impaired acid excretion — gap or non-gap), DKA (ketoacids, HAGMA), lactic acidosis (sepsis/shock/ischemia/metformin, HAGMA)

RF: diabetes · sepsis/shock/hypoperfusion · CKD/ESRD · toxic ingestion · diarrhea · metformin use (esp with AKI)

Data: ABG/VBG + BMP (low HCO3⁻, low pH; confirm primary metabolic acidosis) · anion gap = Na − (Cl + HCO3) (normal ~8–12; correct for albumin: +2.5 per 1 g/dL below 4) · delta-delta (ΔAG/ΔHCO3) (~1–2 pure HAGMA; <1 concurrent NAGMA; >2 concurrent metabolic alkalosis) · Winter's formula (expected pCO2 = 1.5×HCO3 + 8 ±2) (check respiratory compensation; mismatch = added respiratory disorder) · lactate · glucose + serum/urine ketones (β-hydroxybutyrate) · osmolar gap (↑ → toxic alcohols) · salicylate level · BUN/Cr · urine pH/lytes (RTA workup if NAGMA) · K (acidosis shifts K out)

DDx: HAGMA causes (lactate, ketones, uremia, toxins — GOLDMARK) · NAGMA causes (diarrhea vs RTA — urine anion gap) · respiratory acidosis/mixed (compensation formulas) · metabolic alkalosis coexisting (delta-delta >2)

Home Meds: hold metformin (lactic acidosis, esp with AKI) · hold SGLT2i (euglycemic DKA risk) · review acetazolamide/spironolactone/TPN (NAGMA contributors) · renally dose meds if AKI/CKD

Plan

CONSULT: Nephrology (RTA, severe/refractory acidosis, dialysis, toxic ingestion) · Toxicology/Poison control (methanol/ethylene glycol/salicylate) · ICU (severe acidemia/instability) · Endocrine (refractory DKA)

– Step 1 — confirm + classify: ABG/VBG + BMP; calculate the anion gap (albumin-corrected); HAGMA vs NAGMA splits the entire differential
– Step 2 — check for mixed disorders: delta-delta (concurrent NAGMA or metabolic alkalosis) and Winter's formula (appropriate respiratory compensation vs added respiratory disorder)
– Step 3 — treat the cause (this is the therapy):
  • Lactic acidosis: restore perfusion — treat sepsis/shock (IV fluids, source control, antibiotics, vasopressors to MAP target), correct hypoxia/ischemia; stop metformin; bicarbonate generally not helpful unless pH very low
  • DKA: IV isotonic fluids, IV insulin infusion (0.1 units/kg/h after fluids; do not start if K <3.3 until repleted), aggressive potassium repletion (total-body deplete despite normal/high serum), find/treat trigger, close glucose/K/gap monitoring; transition to SC insulin when gap closed
  • AKI/CKD (uremic) acidosis: treat the kidney injury; oral sodium bicarbonate for chronic CKD acidosis (target HCO3 ≥22); dialysis if severe/refractory or other AEIOU indication
  • NAGMA (diarrhea/RTA): treat losses, oral bicarbonate/citrate replacement; type-specific RTA management
  • Toxic alcohols: fomepizole, dialysis, ± bicarbonate; salicylate: urine alkalinization + dialysis if severe
– Bicarbonate therapy — selective: consider IV sodium bicarbonate for severe acidemia (pH <7.1, or per cause); routine bicarbonate for lactic/ketoacidosis is generally not beneficial and can harm (watch Na, volume, ionized Ca, paradoxical intracellular acidosis)
– Monitor K closely — acidosis shifts K extracellularly (serum may mask total-body depletion, esp DKA); treatment shifts it back
– Always check the gap, the delta-delta, and the compensation — a "simple" low bicarb often hides a second (or third) disorder, and missing the mixed picture changes management entirely.
– PT/OT: per underlying illness
– Trend: serial ABG/VBG + bicarbonate + gap, lactate, glucose/ketones (DKA), K + electrolytes, mental status, hemodynamics
– Escalation triggers: pH <7.1 with instability, refractory acidosis, toxic ingestion, or AEIOU → ICU + dialysis/toxicology; worsening despite cause-directed therapy → reassess for mixed/missed cause
– Discharge checklist: cause treated + acid-base normalized/trending; offending drugs addressed (metformin/SGLT2i decision); chronic bicarbonate therapy if CKD; diabetes/sick-day plan if DKA; nephrology/endocrine follow-up; return precautions (rapid breathing, confusion, vomiting, recurrent symptoms)

106. Metabolic Acidosis

complete reference · HAGMA vs NAGMA · anion gap + delta-delta + compensation · AKI/CKD, DKA, lactic acidosis · Full Card

Symptoms / Associated Sx

• The underlying illness often dominates the presentation; Kussmaul respirations (deep, rapid breathing) reflect respiratory compensation

• Nausea, vomiting, abdominal pain, confusion, and lethargy

• Features of the specific cause: polyuria and dehydration in DKA; hypotension and hypoperfusion in lactic acidosis from sepsis/shock; uremic features with AKI/CKD

• Severe acidemia depresses cardiac contractility, predisposes to arrhythmia, and causes vasodilation/hypotension

Neg

• Pt denies vomiting, NG suction, or diuretic use — which would instead generate a metabolic alkalosis (and may coexist as a mixed disorder)

• Pt denies a pure respiratory cause — verify with the pCO2 and the expected compensation

• Pt denies a missed mixed disorder — apply the delta-delta and compensation formulas; denies a toxic alcohol exposure when a high-gap acidosis is otherwise unexplained (check the osmolar gap)

Social History (SHx)

• Diabetes (DKA)

• Alcohol use (alcoholic ketoacidosis, toxic alcohol ingestion, lactic acidosis)

• Toxic ingestions (methanol, ethylene glycol, salicylate)

• CKD/ESRD; diarrhea (NAGMA); metformin use (lactic acidosis, especially with AKI)

Main Etiology / Framework

• High anion gap metabolic acidosis (HAGMA) — "GOLD MARK": Glycols (ethylene glycol, propylene glycol), Oxoproline (pyroglutamic acid, chronic acetaminophen), L-lactate, D-lactate, Methanol, Aspirin (salicylates), Renal failure (retained uremic acids), Ketoacidosis (diabetic, alcoholic, starvation)

• Normal anion gap (hyperchloremic) metabolic acidosis (NAGMA) — "HARDASS": Hyperalimentation, Acetazolamide, Renal tubular acidosis, Diarrhea (the most common cause), Ammonium chloride, Spironolactone, Saline (dilutional)

• Common drivers emphasized here: AKI/CKD impair acid excretion (can be gap or non-gap); DKA produces ketoacids (HAGMA); lactic acidosis arises from sepsis, shock, ischemia, or metformin (HAGMA)

RF

• Modifiable: metformin use in the setting of AKI, glycemic control, perfusion optimization

• Non-modifiable: diabetes, CKD/ESRD, predisposition to sepsis/shock

Data

• ABG/VBG with BMP (low bicarbonate and low pH confirm a primary metabolic acidosis)

• Anion gap = Na − (Cl + HCO3) (normal ~8–12; correct upward by ~2.5 for each 1 g/dL the albumin falls below 4, since hypoalbuminemia lowers the measured gap)

• Delta-delta ratio (ΔAnion gap / ΔHCO3) (~1–2 in a pure HAGMA; <1 suggests a concurrent NAGMA; >2 suggests a concurrent metabolic alkalosis)

• Winter's formula (expected pCO2 = 1.5 × HCO3 + 8 ± 2) (assesses respiratory compensation; a measured pCO2 outside the expected range indicates an additional respiratory disorder)

• Lactate (lactic acidosis)

• Glucose and serum/urine ketones (β-hydroxybutyrate) (ketoacidosis)

• Osmolar gap (an elevated gap suggests toxic alcohols); salicylate level

• BUN/creatinine (uremic acidosis)

• Urine pH, urine electrolytes, urine anion gap (distinguish renal tubular acidosis from GI bicarbonate loss in NAGMA)

• Potassium (acidosis shifts potassium extracellularly, which can mask total-body depletion)

DDx

HAGMA causes (lactate, ketones, uremia, toxins — the GOLD MARK list) · NAGMA causes (diarrhea vs renal tubular acidosis — distinguished by the urine anion gap) · respiratory or mixed acid-base disorder (compensation formulas) · coexisting metabolic alkalosis (delta-delta >2)

Home Meds

• Hold: metformin (lactic acidosis risk, especially with AKI)

• Hold: SGLT2 inhibitors (euglycemic DKA risk during acute illness)

• Review: acetazolamide, spironolactone, and TPN as NAGMA contributors

• Renally dose medications if AKI/CKD is present

Plan

CONSULT: Nephrology (renal tubular acidosis, severe or refractory acidosis, dialysis, toxic ingestion) · Toxicology/Poison Control (methanol, ethylene glycol, salicylate) · ICU (severe acidemia or instability) · Endocrinology (refractory DKA)

• Step 1 — confirm and classify: obtain an ABG/VBG with a BMP and calculate the albumin-corrected anion gap; the HAGMA-versus-NAGMA distinction organizes the entire differential

• Step 2 — check for mixed disorders: apply the delta-delta ratio (to detect a concurrent NAGMA or metabolic alkalosis) and Winter's formula (to confirm appropriate respiratory compensation versus an added respiratory disorder)

• Step 3 — treat the underlying cause, which is the definitive therapy:

• • Lactic acidosis: restore perfusion — treat sepsis/shock with IV fluids, source control, antibiotics, and vasopressors to a MAP target; correct hypoxia and ischemia; stop metformin; bicarbonate is generally unhelpful unless the pH is very low

• • DKA: IV isotonic fluids, an IV insulin infusion (0.1 units/kg/h after initial fluids; do not start insulin if potassium is <3.3 mmol/L until repleted), aggressive potassium repletion (total-body potassium is depleted despite a normal or high serum value), identification and treatment of the trigger, and close monitoring of glucose, potassium, and the anion gap; transition to subcutaneous insulin once the gap has closed

• • AKI/CKD (uremic) acidosis: treat the kidney injury; for chronic CKD metabolic acidosis use oral sodium bicarbonate targeting a serum bicarbonate ≥22 mmol/L; dialyze for severe or refractory acidosis or other dialysis indications

• • NAGMA (diarrhea or RTA): address ongoing losses and replace base with oral sodium bicarbonate or citrate, with type-specific management for renal tubular acidosis

• • Toxic alcohols: fomepizole and dialysis (with bicarbonate as adjunct); for salicylate toxicity, urine alkalinization and hemodialysis for severe poisoning

• Bicarbonate therapy is selective: consider IV sodium bicarbonate for severe acidemia (pH <7.1, or as dictated by the cause); routine bicarbonate for lactic acidosis or ketoacidosis is generally not beneficial and may harm (watch sodium, volume status, ionized calcium, and the risk of paradoxical intracellular acidosis)

• Monitor potassium closely: acidosis shifts potassium out of cells so the serum value can mask total-body depletion (notably in DKA), and treatment shifts it back intracellularly

• PT/OT: guided by the underlying illness

• Trend: serial ABG/VBG with bicarbonate and the anion gap, lactate, glucose and ketones (in DKA), potassium and other electrolytes, mental status, and hemodynamics

• Escalation triggers: pH <7.1 with instability, refractory acidosis, a toxic ingestion, or any AEIOU dialysis indication → ICU with dialysis/toxicology; worsening despite cause-directed therapy → reassess for a mixed or missed cause

• Discharge checklist: the cause treated and the acid-base status normalized or trending toward normal; offending drugs addressed (metformin/SGLT2 inhibitor decisions); chronic oral bicarbonate therapy arranged for CKD acidosis; a diabetes sick-day plan if DKA; nephrology or endocrinology follow-up; return precautions for rapid breathing, confusion, vomiting, or recurrent symptoms

Red Flags

• Severe acidemia (pH <7.1) with hemodynamic instability → ICU; consider bicarbonate and dialysis

• Elevated osmolar gap with a high anion gap → toxic alcohol ingestion → fomepizole and dialysis emergently

• DKA with potassium <3.3 → replete potassium before insulin to avoid fatal hypokalemia

• Lactic acidosis from sepsis/ischemia → the lactate reflects a perfusion emergency, not a number to "buffer"

• Mixed disorder masking severity → always run the delta-delta and compensation checks

Senior IM Resident Pearls

• Always do three calculations, not one: the anion gap (albumin-corrected), the delta-delta, and Winter's formula. A "simple" low bicarbonate frequently hides a second or third acid-base disorder.

• Correct the gap for albumin. Each 1 g/dL drop in albumin lowers the measured gap by ~2.5 — an uncorrected gap can hide a real HAGMA in a hypoalbuminemic patient.

• The treatment is the cause, not the bicarbonate. For lactic acidosis and DKA, restoring perfusion and giving insulin/fluids fix the acidosis; routine bicarbonate doesn't help and can harm.

• Watch the potassium in DKA like a hawk. The serum value overstates total-body stores; insulin and fluids drop it fast, and a low-normal potassium before insulin is a trap.

• An unexplained high-gap acidosis with an osmolar gap is a toxic alcohol until proven otherwise — start fomepizole and call toxicology rather than waiting for levels.

• Urine anion gap separates diarrhea from RTA in a non-gap acidosis — negative (appropriate ammonium excretion) points to GI loss, positive points to renal acidification failure.

• Common mistake: giving bicarbonate to "fix the number" in lactic acidosis — it can worsen intracellular pH and distract from the real fix, which is perfusion.

Nephrology / Urology — Obstructive Uropathy

107. Post-Renal AKI / Obstructive Uropathy

BPH / stones / malignancy · the most reversible AKI · bladder scan + renal US fast · decompress (Foley vs stent/nephrostomy) · watch post-obstructive diuresis · Super Compact

Sx: ↓ or absent urine output (anuria suggests bilateral or single-kidney obstruction); suprapubic fullness/pain (retention), flank pain (upper-tract/stones, colicky) · LUTS (hesitancy, weak stream, frequency — BPH) · hematuria (stones/malignancy) · can be painless (gradual malignant obstruction) (anuria + AKI → exclude obstruction immediately)

Neg: denies pre-renal pattern (hypovolemia, FENa low, bland urine, no hydronephrosis) · denies intrinsic ATN/GN (casts, urine findings) · denies bladder scan low + no hydronephrosis (argues against obstruction) · denies infected obstruction missed (fever + obstruction = emergency)

SHx: older male + BPH/prostate sx (BPH) · stone history/dehydration (calculi) · pelvic/GU/colorectal malignancy or radiation (extrinsic) · anticholinergics/opioids (retention) · neurogenic bladder

Etiology: lower tract: BPH (#1 in older men), prostate cancer, bladder outlet obstruction, neurogenic bladder, clot/stricture · upper tract (must be bilateral or solitary kidney to cause AKI): stones, ureteral/pelvic malignancy, retroperitoneal fibrosis/mass, extrinsic compression; obstruction → ↑ tubular pressure → ↓ GFR (reversible early; permanent if prolonged)

RF: older male/BPH · prior stones · pelvic malignancy/radiation · neurogenic bladder · anticholinergic/opioid use · single functioning kidney

Data: bladder scan / post-void residual (high PVR = retention — immediate, bedside; place Foley) · renal US (hydronephrosis/hydroureter, level, stones, bladder; may be absent early or with encasement) · BMP (↑Cr; K — hyperkalemia common; bicarbonate — may have type 4 RTA/NAGMA) · UA (hematuria — stones/malignancy; pyuria/nitrites — infected obstruction) · CT abd/pelvis (non-contrast for stones; with contrast for mass) (level + cause — stone, mass, hydronephrosis, RP process) · urine cytology/cystoscopy if malignancy · PSA if indicated

DDx: pre-renal AKI (volume, FENa, no hydronephrosis) · intrinsic AKI (ATN/GN) (casts, sediment) · obstruction level — lower vs upper (bladder scan vs hydronephrosis) · infected obstruction (fever + obstruction — emergency)

Home Meds: hold anticholinergics/opioids/alpha-agonists (worsen retention) · start alpha-blocker (tamsulosin (Flomax) 0.4 mg) for BPH retention · renally dose meds · hold nephrotoxins

Plan

CONSULT: Urology (decompression, stones, BPH, malignancy, retention management) · IR (percutaneous nephrostomy if ureteral) · Nephrology (if AKI severe/uncertain) · Oncology (malignant obstruction)

– First: exclude infected obstruction (a urologic emergency): fever + obstruction + pyuria → obstructed infected system = emergent decompression + antibiotics (sepsis bundle, broad-spectrum — piperacillin-tazobactam (Zosyn) 4.5 g IV q6h — and drain via nephrostomy or stent urgently)
– Treat hyperkalemia/life threats first if present (calcium gluconate 1–2 g IV for ECG changes, insulin 10 units IV + D50 25 g, albuterol neb; dialysis if refractory)
– Decompress by level (definitive):
  • Lower tract (retention, high bladder PVR): urethral Foley catheter immediately (suprapubic if urethral catheterization fails — urology); relieves retention and the AKI
  • Upper tract (bilateral hydronephrosis or solitary kidney): ureteral stent (urology) or percutaneous nephrostomy (IR) to decompress
– BPH: Foley + alpha-blocker (tamsulosin (Flomax) 0.4 mg PO daily) ± 5-alpha-reductase inhibitor (finasteride) for size reduction over time; trial of void/urology follow-up; definitive procedure (TURP) for refractory
– Stones causing obstruction: per stone size/location — urology for stent/decompression if obstructing + infected or AKI; analgesia; medical expulsive therapy (tamsulosin) for small distal stones if uninfected
– Malignancy: decompress (stent/nephrostomy), staging, oncology/urology; relieve obstruction before chemo
– Anticipate & manage POST-OBSTRUCTIVE DIURESIS: after relieving high-grade obstruction, monitor UOP/electrolytes closely; if large diuresis with hypovolemia/electrolyte loss → replace ~half the urine output with IV fluid and replete K/Mg; most physiologic diuresis is self-limited — avoid over-replacing (perpetuates it)
– Obstruction is the AKI you can cure at the bedside in minutes with a Foley — bladder scan every unexplained AKI/anuria before the rest of the workup.
– PT/OT: mobilize as tolerated
– Trend: UOP (closely post-decompression), Cr recovery, K + electrolytes (during diuresis), volume status, infection markers
– Escalation triggers: infected obstruction/urosepsis → emergent decompression + ICU; failure to decompress lower tract → urology for suprapubic; brisk post-obstructive diuresis with instability → aggressive monitoring/replacement; non-recovering Cr → prolonged obstruction/intrinsic damage
– Discharge checklist: obstruction relieved + cause addressed (BPH meds, stone plan, malignancy pathway); catheter plan (indwelling vs voiding trial) + urology follow-up; Cr recovery documented; electrolytes stabilized post-diuresis; return precautions (no urine, fever, flank pain, inability to void)

107. Post-Renal AKI / Obstructive Uropathy

complete reference · BPH + stones + malignancy · bladder scan/US → decompress · post-obstructive diuresis · Full Card

Symptoms / Associated Sx

• Decreased or absent urine output — anuria implies bilateral obstruction or obstruction of a single functioning kidney

• Suprapubic fullness and pain (urinary retention) or flank pain (upper-tract obstruction, often colicky with stones)

• Lower urinary tract symptoms (hesitancy, weak stream, frequency, nocturia) with BPH; hematuria with stones or malignancy

• May be painless when obstruction develops gradually (malignant compression)

Neg

• Pt denies a pre-renal pattern (hypovolemia, low FENa, bland urine, no hydronephrosis) — argues against pre-renal AKI

• Pt denies an intrinsic pattern (granular or RBC casts) — argues against ATN or glomerulonephritis

• Pt denies a low post-void residual with no hydronephrosis — these findings argue against obstruction; and denies fever with obstruction, whose combination is an infected obstructed system (an emergency)

Social History (SHx)

• Older male with BPH or prostate symptoms (BPH)

• Stone history and dehydration (calculi)

• Pelvic, genitourinary, or colorectal malignancy or prior radiation (extrinsic obstruction)

• Anticholinergic or opioid use (urinary retention); neurogenic bladder

Main Etiology

• Lower tract: benign prostatic hyperplasia (the most common cause in older men), prostate cancer, bladder outlet obstruction, neurogenic bladder, blood clot, and urethral stricture

• Upper tract (must be bilateral or involve a solitary functioning kidney to cause AKI): ureteral stones, ureteral or pelvic malignancy, retroperitoneal fibrosis or mass, and extrinsic compression

• Obstruction raises intratubular pressure and reduces GFR; this is reversible if relieved early but causes permanent damage if prolonged

RF

• Modifiable: anticholinergic/opioid use, hydration and stone prevention

• Non-modifiable: older age/BPH, prior stones, pelvic malignancy or radiation, neurogenic bladder, a single functioning kidney

Data

• Bladder scan / post-void residual (an immediate bedside test — a high residual indicates retention; place a Foley catheter)

• Renal ultrasound (hydronephrosis and hydroureter, the level of obstruction, stones, and bladder distension; hydronephrosis may be absent very early or when the ureter is encased by tumor/fibrosis)

• BMP (rising creatinine; check potassium — hyperkalemia is common; bicarbonate, as a type 4 RTA/non-gap acidosis can accompany obstruction)

• Urinalysis (hematuria with stones or malignancy; pyuria/nitrites suggest an infected obstruction)

• CT abdomen/pelvis (non-contrast for stones; contrast-enhanced for a mass — defines the level and cause: stone, tumor, hydronephrosis, retroperitoneal process)

• Urine cytology and cystoscopy (when urothelial malignancy is suspected); PSA if indicated

DDx

Pre-renal AKI (volume depletion, low FENa, no hydronephrosis) · intrinsic AKI — ATN or glomerulonephritis (urinary casts and sediment) · lower- vs upper-tract obstruction (bladder scan vs hydronephrosis) · infected obstruction (fever plus obstruction — an emergency)

Home Meds

• Hold: anticholinergics, opioids, and alpha-agonists that worsen retention

• Start: an alpha-blocker (tamsulosin (Flomax) 0.4 mg) for BPH-related retention

• Renally dose medications; hold nephrotoxins

Plan

CONSULT: Urology (decompression, stones, BPH, malignancy, retention management) · Interventional radiology (percutaneous nephrostomy for ureteral obstruction) · Nephrology (severe or uncertain AKI) · Oncology (malignant obstruction)

• First exclude an infected obstruction (a urologic emergency): fever plus obstruction plus pyuria indicates an obstructed, infected collecting system — pursue emergent decompression and antibiotics (sepsis bundle with broad-spectrum coverage such as piperacillin-tazobactam (Zosyn) 4.5 g IV q6h, and urgent drainage via nephrostomy or ureteral stent)

• Treat hyperkalemia and other life threats first when present (calcium gluconate 1–2 g IV for ECG changes, insulin 10 units IV with dextrose 25 g, nebulized albuterol; dialysis if refractory)

• Decompress according to the level, which is the definitive therapy:

• • Lower tract (retention with a high bladder residual): place a urethral Foley catheter immediately, using a suprapubic catheter (urology) if urethral catheterization fails — this relieves the retention and the AKI

• • Upper tract (bilateral hydronephrosis or a solitary kidney): decompress with a ureteral stent (urology) or a percutaneous nephrostomy (IR)

• BPH: Foley plus an alpha-blocker (tamsulosin (Flomax) 0.4 mg PO daily), with a 5-alpha-reductase inhibitor (finasteride) for gland-size reduction over time; arrange a voiding trial and urology follow-up, with TURP for refractory disease

• Obstructing stones: manage by size and location — urology for stenting/decompression if the stone is obstructing with infection or AKI; provide analgesia; medical expulsive therapy with tamsulosin for small distal uninfected stones

• Malignancy: decompress (stent or nephrostomy), obtain staging, and coordinate with oncology and urology, relieving obstruction before chemotherapy

• Anticipate and manage post-obstructive diuresis: after relieving a high-grade obstruction, monitor urine output and electrolytes closely; for a large diuresis with hypovolemia or electrolyte loss, replace roughly half the urine output with IV fluid and replete potassium and magnesium; most physiologic post-obstructive diuresis is self-limited, so avoid over-replacement, which perpetuates it

• PT/OT: mobilize as tolerated

• Trend: urine output (closely after decompression), creatinine recovery, potassium and electrolytes during diuresis, volume status, and infection markers

• Escalation triggers: infected obstruction/urosepsis → emergent decompression and ICU; failure to decompress the lower tract → urology for a suprapubic catheter; brisk post-obstructive diuresis with instability → intensive monitoring and replacement; a creatinine that fails to recover → prolonged obstruction with intrinsic damage

• Discharge checklist: obstruction relieved with the cause addressed (BPH medications, a stone plan, a malignancy pathway); a catheter plan (indwelling vs voiding trial) with urology follow-up; documented creatinine recovery; electrolytes stabilized after any diuresis; return precautions for absent urine output, fever, flank pain, or inability to void

Red Flags

• Infected obstructed system (fever + obstruction + pyuria) → emergent decompression and antibiotics; pus under pressure is a surgical emergency

• Anuria with AKI → exclude obstruction immediately (bilateral or solitary-kidney)

• Hyperkalemia → treat emergently in parallel with decompression

• Brisk post-obstructive diuresis → can cause profound volume and electrolyte depletion

• Hydronephrosis absent despite suspected obstruction → consider early obstruction or ureteral encasement by tumor/retroperitoneal fibrosis (get a CT)

Senior IM Resident Pearls

• Bladder-scan every unexplained AKI. Post-renal AKI is the one you can cure at the bedside in minutes with a Foley — it should be excluded before the elaborate workup.

• Fever plus obstruction is an emergency. An obstructed, infected system won't clear with antibiotics alone — it needs urgent drainage (stent or nephrostomy).

• Upper-tract obstruction needs both sides (or a single kidney) to cause AKI. Unilateral hydronephrosis with a normal contralateral kidney usually won't raise the creatinine — look again if the numbers don't fit.

• Respect the post-obstructive diuresis. After decompressing a high-grade obstruction, replace about half the output and watch electrolytes — but don't chase it, since over-replacement perpetuates it.

• A normal ultrasound doesn't fully exclude obstruction early or with tumor encasement — if the story fits, get a CT.

• Common mistake: launching a full intrinsic-AKI workup before checking a bladder scan and ultrasound — missing a simple, reversible retention.

Cardiology / Nephrology — Cardiorenal Syndrome

108. Cardiorenal Syndrome

CHF → worsening renal function · venous congestion drives it more than low output · decongest (don't reflexively hold diuretics) · the kidney often needs LESS volume, not more · Super Compact

Sx: heart failure signs — dyspnea/orthopnea/PND, edema, JVD, weight gain, rales · with a rising creatinine · poor diuretic response · may have low-output signs (cool extremities, hypotension, fatigue) or predominant congestion (the more common driver) (WRF developing during HF treatment; the kidney is squeezed by venous congestion as much as by low forward flow)

Neg: denies pure pre-renal hypovolemia (would need fluid, not diuresis — assess congestion carefully) · denies obstruction (bladder scan/US) · denies nephrotoxin/contrast/ATN (med review, sediment) · denies that diuretics alone caused it (over-diuresis vs congestion — assess volume)

SHx: heart failure (HFrEF/HFpEF) + baseline renal function · diabetes/HTN/CAD · medication adherence (diuretics, GDMT) · dietary sodium/fluid · prior decompensations

Etiology: bidirectional heart-kidney dysfunction; in acute decompensated HF, worsening renal function (WRF) driven by elevated central venous pressure/renal venous congestion (impairs renal perfusion gradient) > low cardiac output, plus neurohormonal activation (RAAS, SNS), and at times over-diuresis/intravascular depletion; types 1–5 (acute/chronic cardiac→renal, renal→cardiac, systemic)

RF: chronic HF severity · CKD baseline · diabetes/HTN · high venous congestion · RAAS/diuretic interactions · recurrent decompensations

Data: BMP (↑Cr vs baseline; K — diuretics + RAAS shift it; bicarbonate) · BNP/NT-proBNP (HF severity/congestion) · CBC · assess volume/congestion (exam: JVD, edema, weight; CXR — pulmonary edema; POCUS — IVC, B-lines, effusions) · UA/sediment (bland in cardiorenal vs ATN casts) · urine Na (low avid Na retention) · troponin (ischemic trigger) · echo (EF, filling pressures, valves) · daily weights + strict I&Os

DDx: pre-renal from over-diuresis/hypovolemia (volume exam — opposite treatment) · intrinsic ATN (casts, ischemia/contrast) · obstruction (US/bladder scan) · hepatorenal/other low-EAV state (cirrhosis context)

Home Meds: generally CONTINUE diuretics if congested (decongestion improves the kidney) — don't reflexively stop for ↑Cr · GDMT (ACEi/ARB/ARNI, beta-blocker, MRA, SGLT2i) — may tolerate mild Cr rise; hold/adjust if hyperkalemia/hypotension/significant WRF · hold NSAIDs/nephrotoxins

Plan

CONSULT: Cardiology (HF management, advanced therapies) · Nephrology (refractory WRF, ultrafiltration, dialysis) · ICU (cardiogenic shock/inotropes)

– Determine the dominant problem — congestion vs hypoperfusion (exam, weight trend, POCUS/IVC, BP, perfusion): this dictates opposite therapies
– If congested (most common): decongest — don't stop diuretics for a rising Cr; IV loop diuretic (furosemide (Lasix) IV at ≥1–2.5× the home oral dose; bolus or continuous infusion) targeting net negative balance and symptom relief; add a thiazide (metolazone 2.5–5 mg or IV chlorothiazide) for diuretic resistance (sequential nephron blockade); a modest Cr rise during effective decongestion is often acceptable and predicts better outcomes
– If hypoperfused/low-output (cool, hypotensive, low cardiac output): improve forward flow — inotropes (dobutamine or milrinone) ± vasodilators, treat the cause; cardiology/ICU; consider mechanical support in cardiogenic shock
– Optimize neurohormonal therapy: continue/initiate GDMT as BP/K allow — SGLT2 inhibitor (dapagliflozin/empagliflozin — cardio-renal protective, reduces HF events); ACEi/ARB/ARNI and MRA with K monitoring; tolerate small Cr increases on RAAS
– Refractory congestion / diuretic resistance: escalate diuretics, sequential blockade, then ultrafiltration (mechanical fluid removal) or dialysis if refractory/AEIOU
– Treat precipitants: ischemia, arrhythmia (AF/rate), valvular disease, nonadherence, infection, NSAID use
– Avoid the trap: distinguish true intravascular depletion (over-diuresed → needs to ease diuresis) from congestion (needs more decongestion) — they look superficially similar but are opposite
– In congested cardiorenal syndrome, a rising creatinine during effective diuresis is usually NOT a reason to stop — venous decongestion improves renal perfusion, and stopping diuretics often makes both the heart and kidney worse.
– PT/OT: mobilize as tolerated; cardiac rehab consideration
– Trend: daily weight + strict I&Os (the key metric), Cr/BUN, K + electrolytes, BP, symptoms/congestion (JVD, edema, O2), diuretic response (urine output, urine Na)
– Escalation triggers: cardiogenic shock/hypoperfusion → inotropes + ICU; diuretic-refractory congestion → ultrafiltration/nephrology; refractory hyperkalemia/acidosis/uremia/overload → dialysis; worsening despite decongestion → reassess (ATN, obstruction, wrong volume call)
– Discharge checklist: euvolemia achieved + dry weight documented; oral diuretic regimen optimized; GDMT maximized (ACEi/ARB/ARNI, beta-blocker, MRA, SGLT2i) with renal/K monitoring plan; sodium/fluid restriction + daily weight education; early follow-up (cardiology + labs in ~1 wk); nephrology if CKD; return precautions (weight gain, dyspnea, swelling, lightheadedness)

108. Cardiorenal Syndrome

complete reference · CHF causing worsening renal function · congestion-driven physiology · decongestion + GDMT + ultrafiltration · Full Card

Symptoms / Associated Sx

• Signs of heart failure — dyspnea, orthopnea, paroxysmal nocturnal dyspnea, peripheral edema, elevated JVD, weight gain, and pulmonary rales — accompanied by a rising creatinine

• Poor response to diuretics (diuretic resistance)

• Low-output features in some patients (cool extremities, hypotension, fatigue), though predominant congestion is the more common driver of renal dysfunction

Neg

• Pt denies true pre-renal hypovolemia — which would require fluids rather than diuresis, so the congestion assessment must be careful and deliberate

• Pt denies obstruction (bladder scan/ultrasound) and denies a nephrotoxin/contrast/ATN picture (medication review, urine sediment)

• Pt denies that over-diuresis alone caused the rise — distinguishing intravascular depletion from venous congestion is central, as they demand opposite therapies

Social History (SHx)

• Heart failure (reduced or preserved ejection fraction) with the baseline renal function

• Diabetes, hypertension, coronary artery disease

• Medication adherence (diuretics and guideline-directed therapy) and dietary sodium/fluid intake

• Prior decompensations

Main Etiology

• Bidirectional heart–kidney dysfunction in which disease of one organ drives dysfunction of the other

• In acute decompensated heart failure, worsening renal function is driven more by elevated central venous pressure and renal venous congestion (which reduces the perfusion gradient across the kidney) than by low cardiac output, with neurohormonal activation (RAAS, sympathetic nervous system) compounding it; over-diuresis with intravascular depletion contributes in some patients

• Classified into five types (acute and chronic cardiac→renal, acute and chronic renal→cardiac, and secondary/systemic)

RF

• Modifiable: dietary sodium/fluid, medication adherence, congestion management

• Non-modifiable: chronic heart failure severity, baseline CKD, diabetes/hypertension, recurrent decompensations

Data

• BMP (rising creatinine versus baseline; potassium, which both diuretics and RAAS therapy shift; bicarbonate)

• BNP/NT-proBNP (heart failure severity and degree of congestion)

• CBC (anemia, infection)

• Volume/congestion assessment (exam — JVD, edema, weight trend; chest radiograph — pulmonary edema; point-of-care ultrasound — IVC, B-lines, effusions)

• Urinalysis and sediment (bland in cardiorenal syndrome versus granular casts in ATN)

• Urine sodium (low, reflecting avid sodium retention)

• Troponin (an ischemic precipitant)

• Echocardiography (ejection fraction, filling pressures, valvular disease)

• Daily weights and strict intake/output (the central metric for decongestion)

DDx

Pre-renal AKI from over-diuresis/hypovolemia (volume exam — opposite treatment) · intrinsic ATN (casts, ischemia/contrast) · obstruction (ultrasound, bladder scan) · hepatorenal or other low-effective-arterial-volume state (cirrhosis context)

Home Meds

• Generally continue diuretics when the patient is congested — decongestion improves renal function, so do not reflexively stop them for a rising creatinine

• Guideline-directed medical therapy: ACEi/ARB/ARNI, beta-blocker, mineralocorticoid receptor antagonist, and SGLT2 inhibitor — a mild creatinine rise is often tolerable; hold or adjust for hyperkalemia, hypotension, or significant worsening renal function

• Hold: NSAIDs and other nephrotoxins

Plan

CONSULT: Cardiology (heart failure management and advanced therapies) · Nephrology (refractory worsening renal function, ultrafiltration, dialysis) · ICU (cardiogenic shock requiring inotropes/mechanical support)

• Determine the dominant problem — congestion versus hypoperfusion — using the exam, weight trend, point-of-care ultrasound/IVC, blood pressure, and perfusion, because the two require opposite therapies

• If congested (the most common scenario): decongest, and do not stop diuretics for a rising creatinine — give an IV loop diuretic (furosemide (Lasix) IV at ≥1–2.5 times the home oral dose, by bolus or continuous infusion) targeting net negative fluid balance and symptom relief; add a thiazide (metolazone 2.5–5 mg PO or IV chlorothiazide) for diuretic resistance via sequential nephron blockade; a modest creatinine rise during effective decongestion is often acceptable and is associated with better outcomes

• If hypoperfused/low-output (cool, hypotensive, low cardiac output): improve forward flow with inotropes (dobutamine or milrinone) with or without vasodilators, treat the underlying cause, involve cardiology/ICU, and consider mechanical circulatory support in cardiogenic shock

• Optimize neurohormonal therapy: continue or initiate guideline-directed therapy as blood pressure and potassium allow — an SGLT2 inhibitor (dapagliflozin or empagliflozin) for its cardiorenal protection and reduction in heart-failure events; ACEi/ARB/ARNI and an MRA with potassium monitoring, tolerating small creatinine increases on RAAS blockade

• Refractory congestion/diuretic resistance: escalate diuretic dosing and sequential nephron blockade, then proceed to ultrafiltration (mechanical fluid removal) or dialysis for refractory cases or other dialysis indications

• Treat precipitants: ischemia, arrhythmia (atrial fibrillation/rate control), valvular disease, nonadherence, infection, and NSAID use

• Avoid the central trap: distinguish true intravascular depletion from over-diuresis (which needs the diuresis eased) from venous congestion (which needs more decongestion) — they appear superficially similar but call for opposite actions

• PT/OT: mobilize as tolerated; consider cardiac rehabilitation

• Trend: daily weight and strict intake/output (the key metric), creatinine/BUN, potassium and electrolytes, blood pressure, congestion (JVD, edema, oxygenation), and diuretic response (urine output and urine sodium)

• Escalation triggers: cardiogenic shock/hypoperfusion → inotropes and ICU; diuretic-refractory congestion → ultrafiltration and nephrology; refractory hyperkalemia, acidosis, uremia, or overload → dialysis; worsening despite decongestion → reassess for ATN, obstruction, or a misjudged volume state

• Discharge checklist: euvolemia achieved with a documented dry weight; an optimized oral diuretic regimen; maximized guideline-directed therapy (ACEi/ARB/ARNI, beta-blocker, MRA, SGLT2 inhibitor) with a renal/potassium monitoring plan; sodium and fluid restriction with daily weight education; early follow-up (cardiology and labs within about a week); nephrology follow-up if CKD; return precautions for weight gain, dyspnea, swelling, or lightheadedness

Red Flags

• Cardiogenic shock (hypotension, hypoperfusion, end-organ dysfunction) → inotropes, ICU, mechanical support

• Refractory congestion despite escalating diuretics → ultrafiltration

• Hyperkalemia on RAAS therapy plus worsening renal function → adjust therapy and treat the potassium

• Flash pulmonary edema → aggressive decongestion, vasodilators, and ventilatory support

• Worsening renal function that continues after euvolemia → reconsider ATN, obstruction, or an alternative diagnosis

Senior IM Resident Pearls

• Congestion, not low flow, usually drives the kidney down. High renal venous pressure chokes the perfusion gradient — which is why decongesting a wet patient typically improves the creatinine.

• Don't stop diuretics for a rising creatinine in a congested patient. A modest creatinine bump during effective decongestion is expected and predicts better outcomes; stopping diuretics makes both organs worse.

• The hard call is wet versus dry. Over-diuresed depletion and venous congestion look similar but need opposite treatment — use the JVD, weight trend, and IVC to decide.

• Sequential nephron blockade beats diuretic resistance. Adding metolazone or IV chlorothiazide to a loop diuretic unlocks diuresis when the loop alone stalls.

• SGLT2 inhibitors are now core therapy — they protect both heart and kidney and reduce heart-failure events; continue them through most admissions.

• Ultrafiltration is the answer to true diuretic resistance — mechanical fluid removal when escalating diuretics fail, rather than simply accepting congestion.

• Common mistake: reflexively giving IV fluids or holding diuretics because the creatinine rose — in congestive cardiorenal syndrome that worsens the congestion and the kidney; treat the volume state you actually find.